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        <title>European Neuropsychopharmacology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'European Neuropsychopharmacology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=European+Neuropsychopharmacology&t=European+Neuropsychopharmacology&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 15:11:05 +0100</lastBuildDate>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3325421&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000313%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
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            <pubDate>Wed, 03 Mar 2010 15:26:07 +0100</pubDate>
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        <item>
            <title>ECNP Announcement: ECNP Incentives for Young Scientists</title>
            <link>http://www.medworm.com/index.php?rid=3325420&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000325%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
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            <pubDate>Wed, 03 Mar 2010 15:26:07 +0100</pubDate>
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        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=3325419&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000295%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325419</comments>
            <pubDate>Wed, 03 Mar 2010 15:26:07 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3325410&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X1000026X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325410</comments>
            <pubDate>Wed, 03 Mar 2010 15:26:06 +0100</pubDate>
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        <item>
            <title>How much more effective do depot antipsychotics have to be compared to oral antipsychotics before they are prescribed?</title>
            <link>http://www.medworm.com/index.php?rid=3325418&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000052%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antipsychotic depots are less frequently prescribed than oral compounds. In an experimental study involving N=106 psychiatrists we studied how much more effective with respect to relapse prevention depot antipsychotics have to be compared to oral antipsychotics before they are chosen for prescription.Most psychiatrists have to judge depot as clearly superior with respect to relapse prevention before they recommend it to patients. If psychiatrists judge depot as unpleasant for the patients and do not see much need for checking their patients' compliance they are less likely to prescribe depot. Other psychiatrist-related factors (e.g. age, gender, and work experience) did not influence attitudes toward depot. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325418</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Mapping the brain pathways of traumatic memory: Inactivation of protein kinase M zeta in different brain regions disrupts traumatic memory processes and attenuates traumatic stress responses in rats</title>
            <link>http://www.medworm.com/index.php?rid=3325416&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000027%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Predator scent related memories are located in different brain areas at different times beginning with an initial hippocampus-dependent consolidation process, and are eventually stored in the IC. These bring the IC to the forefront as a potential region of significance in processes related to traumatic stress-induced disorders. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325416</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3226315&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X1000012X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226315</comments>
            <pubDate>Mon, 01 Feb 2010 16:23:42 +0100</pubDate>
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        <item>
            <title>ECNP Announcement: Call for Symposium Proposals, Paris, 2010</title>
            <link>http://www.medworm.com/index.php?rid=3226314&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000131%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226314</comments>
            <pubDate>Mon, 01 Feb 2010 16:23:42 +0100</pubDate>
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        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=3226313&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000106%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226313</comments>
            <pubDate>Mon, 01 Feb 2010 16:23:42 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3226304&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000076%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226304</comments>
            <pubDate>Mon, 01 Feb 2010 16:23:40 +0100</pubDate>
            <guid isPermaLink="false">3226304</guid>        </item>
        <item>
            <title>Endogenous cannabinoids in post-mortem brains of Cloninger type 1 and 2 alcoholics</title>
            <link>http://www.medworm.com/index.php?rid=3325415&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000040%2Fabstract%3Frss%3Dyes</link>
            <description>This study analyzed post-mortem brain regions of Cloninger type 1 (n=9) and 2 (n=8) alcoholics and non-alcoholic controls (n=10) for ECs by quantitative liquid chromatography with triple quadrupole mass spectrometric detection. A significant difference was found in anandamide (AEA) levels in nucleus accumbens (NAcc) between the three groups (p=0.047). AEA levels were significantly lower when compared to controls in both perigenual anterior cingulate (p=0.017) and frontal cortices (p=0.018) of type 1 alcoholics. Similar trends were observed for dihomo-γ-linolenoyl ethanolamide and docosahexaenoyl ethanolamide, but not for 2-arachidonoylglycerol, palmitoyl ethanolamide, or oleoyl ethanolamide. Although preliminary, and from diagnostic groups with a relatively small number of subjects and su...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325415</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3325415</guid>        </item>
        <item>
            <title>Deletion variant of α2b-adrenergic receptor gene moderates the effect of COMT val158met polymorphism on episodic memory performance</title>
            <link>http://www.medworm.com/index.php?rid=3325417&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X10000039%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we demonstrate an interaction between this COMT polymorphism and a deletion variant of ADRA2B, the gene encoding the α2b-adrenergic receptor on episodic memory performance. Specifically, carriage of the ADRA2B deletion abolished the relative memory impairment in homozygous COMT val158 carriers compared to met158 carriers. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325417</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3325417</guid>        </item>
        <item>
            <title>The multifaceted effects of oral administration of methylphenidate in juvenile rats: Anxiety, activity, and attention</title>
            <link>http://www.medworm.com/index.php?rid=3325414&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002818%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In previous studies, acutely administered oral methylphenidate (MPD, 3mg/kg) prior to testing improved performance on the radial arm maze in juvenile rats. In order to examine the mechanisms producing this improvement we administered MPD once prior to each test of anxiety, locomotor activity and attention. On postnatal day (PND) 22 on an elevated plus maze, rats spent more time beyond the rails on the open arms and showed altered risk-assessment behaviors suggesting an anxiolytic-like effect of MPD. Grid crossings on the plus maze indicated that MPD increased locomotor activity, as did activity recording on PND 23. In another group of juveniles, MPD improved performance in a multi-trial attention task in an age-dependent fashion. These data suggest that oral MPD has multifaceted ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325414</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Memory in humans is unaffected by central H1-antagonism, while objectively and subjectively measured sedation is increased</title>
            <link>http://www.medworm.com/index.php?rid=3325413&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002806%2Fabstract%3Frss%3Dyes</link>
            <description>This study aimed to determine whether a centrally active antihistamine impairs memory performance and to dissociate such effects from sedation. Eighteen healthy volunteers received single oral doses of dexchlorpheniramine 4mg, lorazepam 1mg and placebo in a 3-way, double blind, crossover designed study. The active control lorazepam impaired episodic- and working memory performance and increased sedation, while dexchlorpheniramine only increased sedation. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325413</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Chronic effects of cannabis use on the human reward system: An fMRI study</title>
            <link>http://www.medworm.com/index.php?rid=3226307&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002612%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cannabis is one of the most used drugs of abuse. It affects the brain reward system in animals, and has proven rewarding and addictive potential in humans. We used functional MRI to measure brain activity during reward anticipation in a monetary reward task. Long-term cannabis users were compared to healthy controls. An additional control group consisting of nicotine users was included. Cannabis users showed attenuated brain activity during reward anticipation in the nucleus accumbens compared to non-smoking controls, but not compared to smoking controls. Cannabis users showed decreased reward anticipation activity in the caudate nucleus, compared to both non-smoking and smoking controls. These data suggest that nicotine may be responsible for attenuated reward anticipation activ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226307</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226307</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3151370&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002892%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151370</comments>
            <pubDate>Fri, 08 Jan 2010 15:10:27 +0100</pubDate>
            <guid isPermaLink="false">3151370</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=3151369&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002879%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151369</comments>
            <pubDate>Fri, 08 Jan 2010 15:10:27 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3151360&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002843%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151360</comments>
            <pubDate>Fri, 08 Jan 2010 15:10:26 +0100</pubDate>
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        <item>
            <title>Late potentials in the signal-averaged electrocardiogram in schizophrenia patients maintained on antipsychotic agents: A preliminary naturalistic study</title>
            <link>http://www.medworm.com/index.php?rid=3226306&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002788%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In the present, preliminary, naturalistic study, cardiac ventricular late potentials (LPs), were measured in 33 physically healthy schizophrenia patients (13 — females and 26 — males, age — 45.5±8.8years) maintained on typical and atypical antipsychotic agents. These LPs represent delayed ventricular activation that might predispose to fatal ventricular arrhythmias and sudden cardiac death (SCD) in cardiac patients. Sixteen of the 33 patients (∼48%) were found to be positive for LPs (compared to 3.7–6% in the general population). No association was found with any of the following: drug type, anti-cholinergic burden, daily dose of antipsychotic agents, age, gender, disease duration, QTc interval and QT dispersion. Further large-scale longitudinal prospective studies are...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226306</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226306</guid>        </item>
        <item>
            <title>The risk of death among adult participants in trials of antipsychotic drugs in schizophrenia1</title>
            <link>http://www.medworm.com/index.php?rid=3226305&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900279X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In this paper we investigate mortality in short-term placebo-controlled trials conducted to demonstrate efficacy and safety of atypical antipsychotic drugs for the treatment of schizophrenic patients in the acute phase of illness. Arguments are provided, why short-term placebo-controlled studies are required.This is an integrated analysis of results from randomized placebo-controlled trials conducted pre-licensing for risperidone, olanzapine, quetiapine IR, ziprasidone, risperidone consta, aripiprazole, paliperidone, and quetiapine XR. Information was retrieved from study publications, EPAR, and from the FDA SBA, all in the public domain.7553 patients were randomized in the remaining 23 short-term acute phase clinical trials. 2/5738 patients died after having been randomized to a...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226305</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226305</guid>        </item>
        <item>
            <title>(+)-UH 232, a partial agonist of the D3 dopamine receptors, attenuates cognitive effects of angiotensin IV and des-Phe6-angiotensin IV in rats</title>
            <link>http://www.medworm.com/index.php?rid=3325412&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002776%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we evaluated role of the presynaptic DA D3 receptors in these effects. For that purpose effect of (+)-UH 232, a selective D3 DA receptors partial agonist preferring presynaptic sites, on the pro-cognitive action of intracerebroventricularly (icv) injected Ang IV and des-Phe6-Ang IV was examined. Male Wistar rats weighing 180–200g were used. Both peptides given at the dose of 1nmol facilitated recall of a passive avoidance (PA) behaviour, improved object recognition (OR), and increased apomorphine-induced stereotype behaviour. In the auxiliary tests performed to control for the unspecific influence of motor (open field, OF) and emotional (‘plus’ maze, PM) effects of our treatments on the results of the memory tests they had either no (OF) or negligible (PM) effects. Intr...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325412</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>NMDA NR2B subtype-selective receptor antagonists fail to antagonize electrically-precipitated seizures and elicit popping in mice</title>
            <link>http://www.medworm.com/index.php?rid=3226312&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002594%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: NR2B-subtype-selective antagonists differ from MK-801, a nonselective NMDA receptor antagonist. MK-801 antagonizes electrical seizures at doses as low as 0.1 to 0.18mg/kg and elicits popping at doses as low as 0.5mg/kg, whereas ifenprodil and Ro 8-4304 were unable to do so at the doses tested. Ro 25-6981, however, was able to antagonize electrically-precipitated tonic hindlimb extension at 100mg/kg, but was not able to elicit popping behavior at this dose. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226312</comments>
            <pubDate>Mon, 21 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226312</guid>        </item>
        <item>
            <title>Development of the 2nd generation neurokinin-1 receptor antagonist LY686017 for social anxiety disorder</title>
            <link>http://www.medworm.com/index.php?rid=3151362&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002417%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The neurokinin-1 (NK-1) antagonist LY686017 showed activity in preclinical anxiety models. The clinical development of LY686017 included a PET study and a proof-of-concept in social anxiety disorder (SAD). [11C]GR205171 was used healthy volunteers receiving 1–100mg/d LY686017 for 28days to determine brain receptor occupancy (RO). The mean NK-1 RO increased ranged from 25% with 1mg to 93% with 100mg. Subsequently, a 12-week randomized clinical trial tested LY686017 vs. paroxetine, or placebo in SAD. Pharmacokinetic (PK)/RO modeling based on the PET results predicted that once daily dosing of &gt;30mg LY686017 led to sustained trough RO of over 80%. 189 outpatients suffering from SAD were randomly assigned to 12-weeks treatment with 50mg/d LY686017 (N=77), placebo (N=74), or 20mg/d ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151362</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Potential anxiogenic effects of cannabinoid CB1 receptor antagonists/inverse agonists in rats: Comparisons between AM4113, AM251, and the benzodiazepine inverse agonist FG-7142</title>
            <link>http://www.medworm.com/index.php?rid=3151365&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002533%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cannabinoid CB1 inverse agonists suppress food-motivated behaviors, but may also induce psychiatric effects such as depression and anxiety. To evaluate behaviors potentially related to anxiety, the present experiments assessed the CB1 inverse agonist AM251 (2.0–8.0mg/kg), the CB1 antagonist AM4113 (3.0–12.0mg/kg), and the benzodiazepine inverse agonist FG-7142 (10.0–20.0mg/kg), using the open field test and the elevated plus maze. Although all three drugs affected open field behavior, these effects were largely due to actions on locomotion. In the elevated plus maze, FG-7142 and AM251 both produced anxiogenic effects. FG-7142 and AM251 also significantly increased c-Fos activity in the amygdala and nucleus accumbens shell. In contrast, AM4113 failed to affect performance in...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151365</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>A mouse model of anxiety molecularly characterized by altered protein networks in the brain proteome</title>
            <link>http://www.medworm.com/index.php?rid=3151364&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002545%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recently, several attempts have been made to describe changes related to certain anxiety states in the proteome of experimental animal models. However, these studies are restricted by limitations regarding the number and correct identification of separated proteins. Moreover, the application of a systems biology approach to discover the molecular mechanisms of anxiety requires genetically homogenous inbred animal models. Therefore, we developed a novel mouse model of anxiety using a combination of crossbreeding (inbred for 35 generations) and behavioral selection. We found significant changes in 82 proteins in the total brain proteome compared to the control proteome. Thirty-four of these proteins had been previously identified in other anxiety, depression or repeated psychosocia...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151364</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3083841&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002685%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083841</comments>
            <pubDate>Mon, 14 Dec 2009 15:05:55 +0100</pubDate>
            <guid isPermaLink="false">3083841</guid>        </item>
        <item>
            <title>ECNP Announcement: Young Scientists in Amsterdam 2010</title>
            <link>http://www.medworm.com/index.php?rid=3083840&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002752%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083840</comments>
            <pubDate>Mon, 14 Dec 2009 15:05:55 +0100</pubDate>
            <guid isPermaLink="false">3083840</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=3083839&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002661%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083839</comments>
            <pubDate>Mon, 14 Dec 2009 15:05:55 +0100</pubDate>
            <guid isPermaLink="false">3083839</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3083832&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002636%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083832</comments>
            <pubDate>Mon, 14 Dec 2009 15:05:53 +0100</pubDate>
            <guid isPermaLink="false">3083832</guid>        </item>
        <item>
            <title>Evaluation of the effect of selective serotonin-reuptake inhibitors on lymphocyte subsets in patients with a major depressive disorder</title>
            <link>http://www.medworm.com/index.php?rid=3151363&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002569%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: To date, only the effect of a short-term antidepressant treatment ( (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151363</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3151363</guid>        </item>
        <item>
            <title>Erratum to “Effect of basic fibroblast growth factor (FGF2) gene polymorphisms on SSRIs treatment response and side effects” [Eur. Neuropsychopharmacol. 19 (2009) 718–725]</title>
            <link>http://www.medworm.com/index.php?rid=3151368&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002570%2Fabstract%3Frss%3Dyes</link>
            <description>Discussion section. Some text was omitted from the first paragraph. This fully corrected paragraph is reproduced in full below: (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151368</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3151368</guid>        </item>
        <item>
            <title>The nicotinic acetylcholine receptor partial agonist varenicline and the treatment of drug dependence: A review</title>
            <link>http://www.medworm.com/index.php?rid=3151361&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002521%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Drug dependence is a chronic brain disease characterized by recurrent episodes of relapse, even when the person is motivated to quit. Relapse is a major problem and new pharmacotherapies are needed to prevent relapse episodes. The nicotinic acetylcholine receptor (nAChR) plays an important role in nicotine dependence, alcohol consumption and cue-induced cocaine craving. Stimulation of the nAChR has been found to alter and modulate cell firing in brain areas important for the maintenance of drug dependence. Varenicline, an α4β2 nAChR partial agonist and an α7 nAChR full agonist registered for the treatment of nicotine dependence, significantly reduces nicotine craving and prevents relapse. In addition, varenicline reduces alcohol consumption in rats. Based on a review of the av...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151361</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3151361</guid>        </item>
        <item>
            <title>Effects of escitalopram on stress-related relapses in women with multiple sclerosis: An open-label, randomized, controlled, one-year follow-up study</title>
            <link>http://www.medworm.com/index.php?rid=3151366&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002405%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A growing body of evidence supports the association between Stressful Life Events (SLEs) and increased risk for relapse in Multiple Sclerosis (MS). In this open-label, randomized, controlled, one-year prospective study we investigated the effects of escitalopram on stress-related relapses in 48 women with relapsing–remitting MS. Patients were randomly assigned either to receive escitalopram 10mg/day (e-group, N=24) or to continue with treatment as usual, as a control group (c-group, N=24). SLEs were documented weekly in self-report diaries and were classified afterwards as short- or long-term depending on their psychological impact as this was subjectively felt by the patient. The cumulative risk for relapse was 2.9 times higher for controls than for escitalopram-treated patien...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151366</comments>
            <pubDate>Fri, 20 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3151366</guid>        </item>
        <item>
            <title>The effect of chronic antipsychotic drug administration on nitric oxide synthase activity and gene expression in rat penile tissues</title>
            <link>http://www.medworm.com/index.php?rid=3325411&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002387%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antipsychotic drug treatment may be associated with common and problematic sexual dysfunction, especially impotence, which can diminish quality of life and lead to treatment noncompliance. Nitric oxide synthase (NOS) is an important cellular modulator of erectile function. We have therefore investigated the effect of antipsychotic drug on activity and gene expression of NOS in rat penile tissues. The activity of constitutive NOS was significantly suppressed below control by a 21days administration of 1mg/kg haloperidol, which also significantly decreased expression of endothelial NOS (eNOS) and neural NOS mRNA. Risperidone at 0.5mg/kg also reduced eNOS mRNA expression. Haloperidol or risperidone did not change gene expression and activity of inducible NOS (iNOS). Quetiapine signi...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3325411</comments>
            <pubDate>Mon, 16 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3325411</guid>        </item>
        <item>
            <title>CSF neurochemicals during tryptophan depletion in individuals with remitted depression and healthy controls</title>
            <link>http://www.medworm.com/index.php?rid=3083834&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002399%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The purpose of this study was to examine the differential effects of acute tryptophan (TRP) depletion vs. sham condition on plasma, cerebrospinal fluid (CSF) biochemical parameters, and mood in the following three subject groups: (1) nine antidepressant-free individuals with remitted depression, (2) eight paroxetine-treated individuals with recently remitted depression, and (3) seven healthy controls. Plasma TRP decreased during TRP depletion and increased during sham condition (p (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083834</comments>
            <pubDate>Mon, 09 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083834</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2949552&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900248X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949552</comments>
            <pubDate>Mon, 02 Nov 2009 15:20:50 +0100</pubDate>
            <guid isPermaLink="false">2949552</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2949551&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002466%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949551</comments>
            <pubDate>Mon, 02 Nov 2009 15:20:50 +0100</pubDate>
            <guid isPermaLink="false">2949551</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2949541&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002430%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949541</comments>
            <pubDate>Mon, 02 Nov 2009 15:20:47 +0100</pubDate>
            <guid isPermaLink="false">2949541</guid>        </item>
        <item>
            <title>Effects of repeated risperidone exposure on serotonin receptor subtypes in developing rats</title>
            <link>http://www.medworm.com/index.php?rid=3226310&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002326%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we examined the effects of long-term treatment of risperidone on two serotonin receptor subtypes in brain regions of juvenile rat. Levels of 5-HT1A and 5-HT2A receptors in forebrain regions of juvenile rats were quantified after 3weeks of treatment with three different doses of risperidone (0.3, 1.0 and 3.0mg/kg). Findings were compared to previously reported changes in 5-HT receptors after risperidone treatment (3.0mg/kg) in adult rat brain. The three doses of risperidone selectively and dose-dependently increased levels of 5-HT1A receptors in medial–prefrontal and dorsolateral–frontal cortices of juvenile animals. The higher doses (1.0 and 3.0mg/kg) of risperidone also increased 5-HT1A receptor binding in hippocampal CA1 region of juvenile but not adult rats. In contra...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226310</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226310</guid>        </item>
        <item>
            <title>Palmitoylethanolamide modulates pentobarbital-evoked hypnotic effect in mice: Involvement of allopregnanolone biosynthesis</title>
            <link>http://www.medworm.com/index.php?rid=3226311&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002338%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Palmitoylethanolamde (PEA) is an endogenous lipid neuromodulator that mediates a broad spectrum of pharmacological effects by activation of peroxisome proliferator-activated receptor alpha (PPAR-α). Detectable or high levels of PEA in the CNS have been found, but the specific function of this lipid remains to be clarified. Here we report evidence that PEA, activating PPAR-α receptor and involving neurosteroids de novo synthesis, modulates pentobarbital-evoked hypnotic effect. A single i.c.v. administration of PEA (1–5µg) increases pentobarbital induced loss of righting reflex (LORR) duration in mice. This effect is mimicked by GW7647 (3µg), a synthetic PPAR-α agonist, and disappears in PPAR-α knockout mice.Antagonism experiments strongly support the engaging of neurostero...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226311</comments>
            <pubDate>Wed, 28 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226311</guid>        </item>
        <item>
            <title>Cannabinoid self-administration attenuates PCP-induced schizophrenia-like symptoms in adult rats</title>
            <link>http://www.medworm.com/index.php?rid=3083835&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900234X%2Fabstract%3Frss%3Dyes</link>
            <description>We report that WIN self-administration attenuates PCP-induced deficits in (i) prepulse inhibition (PPI) of the acoustic startle reflex, (ii) cognitive skills, and (iii) sociability, suggesting that cannabinoid consumption can ameliorate the schizophrenia-like behavioral alterations caused by PCP. A parallel study performed in animals receiving WIN on a non-voluntary basis (experimenter-given) confirmed an ameliorating effect of cannabinoid administration on the symptoms of schizophrenia induced by PCP. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083835</comments>
            <pubDate>Mon, 26 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083835</guid>        </item>
        <item>
            <title>The development- and phencyclidine-regulated induction of synapse-associated protein-97 gene in the rat neocortex</title>
            <link>http://www.medworm.com/index.php?rid=3226309&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900220X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Using the RNA arbitrarily-primed PCR and the competitive RT-PCR, we have isolated the neocortical transcripts that are upregulated and unchanged in the adult and infant rats, respectively, after a systemic injection of an N-methyl-d-aspartate (NMDA) receptor antagonist phencyclidine (PCP), and found them identical to the synapse-associated protein-97 (SAP97) gene mRNAs. The upregulation of the SAP97 transcripts in the adult neocortex after the acute PCP injection was mimicked by another NMDA antagonist, dizocilpine, but not by the indirect dopamine agonists, methamphetamine and cocaine, a selective D1 receptor antagonist SCH23390, a D2 receptor-preferring antagonist haloperidol and a GABAergic anesthetic pentobarbital. Moreover, the pretreatment with a typical antipsychotic halop...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226309</comments>
            <pubDate>Mon, 19 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226309</guid>        </item>
        <item>
            <title>Antipsychotic effects on auditory sensory gating in schizophrenia patients</title>
            <link>http://www.medworm.com/index.php?rid=2949550&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002314%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: P50 sensory gating deficit has repeatedly been demonstrated in schizophrenia. Studies have produced inconsistent findings with respect to normalization of P50 gating in patients with schizophrenia receiving treatment with different antipsychotics. The current study was designed to determine whether there is a difference in P50 gating in schizophrenia patients treated with first-generation antipsychotics (FGAs) and second-generation antipsychotics (SGAs), including clozapine. P50 evoked potential recordings were obtained from 160 patients with schizophrenia and 77 healthy comparison subjects. Forty-three patients were being treated with clozapine, sixty-eight were taking SGAs (33 risperidone, 21 olanzapine, 11 aripiprazole, and 3 combinations of SGAs) and 49 were being treated wit...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949550</comments>
            <pubDate>Thu, 15 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949550</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2860877&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002272%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860877</comments>
            <pubDate>Mon, 05 Oct 2009 17:32:39 +0100</pubDate>
            <guid isPermaLink="false">2860877</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2860876&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002259%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860876</comments>
            <pubDate>Mon, 05 Oct 2009 17:32:39 +0100</pubDate>
            <guid isPermaLink="false">2860876</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2860867&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002223%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860867</comments>
            <pubDate>Mon, 05 Oct 2009 17:32:38 +0100</pubDate>
            <guid isPermaLink="false">2860867</guid>        </item>
        <item>
            <title>Adult-onset hippocampal-specific neuropeptide Y overexpression confers mild anxiolytic effect in mice</title>
            <link>http://www.medworm.com/index.php?rid=3226308&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002120%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The anticonvulsive properties of neuropeptide Y (NPY) are opening up opportunity for the development of NPY gene transfer as a therapy for epilepsy. In order to pursue the potential clinical translation of this approach, the effects of somatic NPY gene transfer on other hippocampal functions need to be assessed. The present study characterized the behavioral effects of recombinant adeno-associated viral vector (rAAV)-mediated hippocampal NPY overexpression in adult male mice and also Y1 receptor knockout mice. In wild-type mice, there were no obvious adverse effects on the general health, motor function and cognition following rAAV-NPY treatment. Moreover, hippocampal NPY overexpression induced a moderate anxiolytic effect in the open field test and elevated plus maze. Intriguing...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3226308</comments>
            <pubDate>Fri, 25 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3226308</guid>        </item>
        <item>
            <title>HTR2A gene variation is involved in antidepressant treatment response</title>
            <link>http://www.medworm.com/index.php?rid=3083838&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002193%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Two serotonin 2A receptor (HTR2A) SNPs recently reported to be associated with antidepressant treatment response in STAR⁎D (rs7997012; rs1928040) were analyzed for association with treatment response in two independent Caucasian samples of patients with a Major Depressive Episode. In the combined sample (n=637) SNP rs7997012 was significantly associated with remission after five weeks providing first replicative support for the initial finding, with, however, an inverse allelic association as compared to the STAR⁎D sample. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083838</comments>
            <pubDate>Wed, 16 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083838</guid>        </item>
        <item>
            <title>The time course of unconditioned morphine-induced psychomotor sensitization mirrors the phosphorylation of FADD and MEK/ERK in rat striatum: Role of PEA-15 as a FADD-ERK binding partner in striatal plasticity</title>
            <link>http://www.medworm.com/index.php?rid=3083837&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002132%2Fabstract%3Frss%3Dyes</link>
            <description>This study investigated the modulation of FADD and MAP kinase signaling, as well as their interactions with PEA-15 (phosphoprotein enriched in astrocytes—15kDa) and Akt1 pathways, during the expression of unconditioned morphine-induced psychomotor sensitization. In morphine-pretreated rats (10mg/kg during 5days), a challenge dose of the opiate induced a robust psychomotor sensitization at early withdrawal (3days, SW 3), but not after a prolonged abstinence period (14days), which was coincident with an accelerated dopamine turnover in the striatum. Marked concomitant increases in the content of p-FADD (48%) and the activation of MEK-ERK (46–79%) were quantified during the short-term expression of morphine sensitization (SW 3, in the absence of morphine challenge). At SW 3, p-PEA-15, a F...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083837</comments>
            <pubDate>Wed, 16 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083837</guid>        </item>
        <item>
            <title>Regulation of adult neurogenesis by stress, sleep disruption, exercise and inflammation: Implications for depression and antidepressant action</title>
            <link>http://www.medworm.com/index.php?rid=3083833&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002119%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Adult hippocampal neurogenesis, a once unorthodox concept, has changed into one of the most rapidly growing fields in neuroscience. The present report results from the ECNP targeted expert meeting in 2007 during which cellular plasticity changes were addressed in the adult brain, focusing on neurogenesis and apoptosis in hippocampus and frontal cortex. We discuss recent studies investigating factors that regulate neurogenesis with special emphasis on effects of stress, sleep disruption, exercise and inflammation, a group of seemingly unrelated factors that share at least two unifying properties, namely that they all regulate adult hippocampal neurogenesis and have all been implicated in the pathophysiology of mood disorders.We conclude that although neurogenesis has been implicat...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083833</comments>
            <pubDate>Mon, 14 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083833</guid>        </item>
        <item>
            <title>Signs of striatal dopamine transporter density increase in association with improvement of tardive dyskinesia in a patient with schizophrenia, as demonstrated by a DAT scan</title>
            <link>http://www.medworm.com/index.php?rid=3151367&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002107%2Fabstract%3Frss%3Dyes</link>
            <description>We report a case with psychotic and tardive dyskinesia symptoms. A DAT scan showed decreased dopamine transporter uptake in the area of brain's basal gaglia. A trial with quetiapine improved both psychotic and TD symptoms while a second DAT scan showed improvement status. We conclude that increased dopamine transporter uptake seemed to associate with the improvement of TD. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3151367</comments>
            <pubDate>Wed, 09 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3151367</guid>        </item>
        <item>
            <title>Mazindol attenuates ketamine-induced cognitive deficit in the attentional set shifting task in rats</title>
            <link>http://www.medworm.com/index.php?rid=3083836&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001941%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cognitive impairments associated with schizophrenia await an effective treatment. In order to model schizophrenia-like cognitive deficits in rats, we evaluated the effects of ketamine, a dissociative anesthetic NMDA/glutamate receptor channel blocker in the attentional set-shifting task (ASST). Acute administration of ketamine (10 but not 3mg/kg) selectively impaired solving of the extradimensional (ED) set-shifting component. Next, we investigated whether the co-administration of mazindol, a dopamine and norepinephrine reuptake inhibitor would protect rats from ketamine-induced deficits. Mazindol dose-dependently and selectively alleviated ketamine-induced ED deficit with a minimal effective dose of 0.5mg/kg. The ED component improvement was noted primarily in ketamine — but n...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083836</comments>
            <pubDate>Thu, 03 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083836</guid>        </item>
        <item>
            <title>BL-1020, a novel antipsychotic candidate with GABA-enhancing effects: D2 receptor occupancy study in humans</title>
            <link>http://www.medworm.com/index.php?rid=2949543&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001916%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: BL-1020 is a potentially novel antipsychotic, which comprises the typical antipsychotic perphenazine linked by an ester bound to γ-aminobutyric acid (GABA), intending a simultaneous dopamine-2 (D2) receptor blockade and GABA facilitation in the brain. This positron emission tomography (PET) study, using [11C]raclopride, assessed the extent and duration of D2 receptor occupancy (D2 RO) and safety for single doses of BL-1020 in healthy male subjects. Overall, this study did not raise any safety concern. Single doses of 16–32 mg BL-1020 caused a dose dependent striatal D2 RO. The 32 mg dose of BL-1020 resulted in an average D2 RO of 44% at 4–6 h post dosing (pd), which declined to 33% at 24 h pd. Equimolar doses of BL-1020 and perphenazine resulted in similar D2 RO at 24 h...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949543</comments>
            <pubDate>Tue, 01 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949543</guid>        </item>
        <item>
            <title>Brain structural changes associated with chronicity and antipsychotic treatment in schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=2949542&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001928%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Accumulating evidence suggest a life-long impact of disease related mechanisms on brain structure in schizophrenia which may be modified by antipsychotic treatment. The aim of the present study was to investigate in a large sample of patients with schizophrenia the effect of illness duration and antipsychotic treatment on brain structure. Seventy-one schizophrenic patients and 79 age and gender matched healthy participants underwent brain magnetic resonance imaging (MRI). All images were processed with voxel based morphometry, using SPM5. Compared to healthy participants, patients showed decrements in gray matter volume in the left medial and left inferior frontal gyrus. In addition, duration of illness was negatively associated with gray matter volume in prefrontal regions bilat...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949542</comments>
            <pubDate>Tue, 01 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949542</guid>        </item>
        <item>
            <title>Atomoxetine hydrochloride in the treatment of children and adolescents with attention-deficit/hyperactivity disorder and comorbid oppositional defiant disorder: A placebo-controlled Italian study</title>
            <link>http://www.medworm.com/index.php?rid=2860875&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900193X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Objective: The primary aim of this study was to assess the efficacy of atomoxetine in improving ADHD and ODD symptoms in paediatric patients with ADHD and comorbid oppositional defiant disorder (ODD), non-responders to previous psychological intervention with parent support.Methods: This was a multicentre, randomised, placebo-controlled trial conducted in patients aged 6–15 years, with ADHD and ODD diagnosed according to the DSM-IV criteria by a structured clinical interview (K-SADS-PL). Only subjects who are non-responders to a 6-week standardized parent training were randomised to atomoxetine (up to 1.2 mg/kg/day) or placebo (in a 3:1 ratio) for the following 8-week double blind phase.Results: Only 2 of the 156 patients enrolled for the parent support phase (92.9% of males;...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860875</comments>
            <pubDate>Mon, 31 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860875</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2747002&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900203X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2747002</comments>
            <pubDate>Mon, 31 Aug 2009 12:51:03 +0100</pubDate>
            <guid isPermaLink="false">2747002</guid>        </item>
        <item>
            <title>ECNP Announcement: ECNP 2010 Awards for Outstanding Scientists</title>
            <link>http://www.medworm.com/index.php?rid=2747001&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002089%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2747001</comments>
            <pubDate>Mon, 31 Aug 2009 12:51:03 +0100</pubDate>
            <guid isPermaLink="false">2747001</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2747000&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002016%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2747000</comments>
            <pubDate>Mon, 31 Aug 2009 12:51:02 +0100</pubDate>
            <guid isPermaLink="false">2747000</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2746990&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09002090%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746990</comments>
            <pubDate>Mon, 31 Aug 2009 12:51:01 +0100</pubDate>
            <guid isPermaLink="false">2746990</guid>        </item>
        <item>
            <title>Rejuvenation of antioxidant and cholinergic systems contributes to the effect of procyanidins extracted from the lotus seedpod ameliorating memory impairment in cognitively impaired aged rats</title>
            <link>http://www.medworm.com/index.php?rid=2949544&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001904%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The major purpose of this study was to determine the effect of procyanidins extracted from the lotus seedpod (LSPC) on the learning and memory impairments in cognitively impaired aged rats. Based on Morris water maze performance compared with young female rats, aged unimpaired (AU) and aged impaired (AI) rats were chosen from aged female rats. LSPC supplementation (50, 100 mg/kg BW, p.o.) for 7 weeks significantly improved learning and memory impairments in AI animals in the Morris water maze test, as evaluated by shortened escape latency and swimming distance. Aged rats had significantly declined antioxidant defense capacities and significantly increased lipid peroxidation and protein oxidation levels in hippocampus and cerebral cortex than young rats. Further, AI group had hi...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949544</comments>
            <pubDate>Fri, 28 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949544</guid>        </item>
        <item>
            <title>Antidepressive behaviors induced byenriched environment might be modulated by glucocorticoid levels</title>
            <link>http://www.medworm.com/index.php?rid=2949546&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001709%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Exposure to enriched environment (EE) can influence expression of depression symptoms, however, the underlying mechanism has not been established, although neurogenesis was probably involved. It has been reported that EE stimulates glucocorticoids release. However, the role of corticosterone (CORT) in effects of EE is still unknown. To address these issues, we examined depression-like behaviors of the animals exposed to EE with low dose CORT supplement following bilateral adrenalectomy (ADX+CORT). Two months after housing, tail suspension test and forced swim test were used to assess depression-related behavior of mice. Serum CORT levels were measured by radio-immunoassay. Signals of DNA synthesis marker bromodeoxyuridine and immature neuronal marker doublecortin were measured by...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949546</comments>
            <pubDate>Fri, 07 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949546</guid>        </item>
        <item>
            <title>Effects of quetiapine on phencyclidine-induced cognitive deficits in mice: A possible role of α1-adrenoceptors</title>
            <link>http://www.medworm.com/index.php?rid=2949545&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001710%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Accumulating evidence suggests that α1-adrenoceptors may be involved in the mechanisms of action of some antipsychotic drugs. The present study was undertaken to examine the effects of quetiapine, an atypical antipsychotic drug with α1-adrenoceptor antagonism, on cognitive deficits in mice after repeated administration of the NMDA receptor antagonist phencyclidine (PCP). Subsequent subchronic (14 days) administration of quetiapine (1.0, 10, or 30 mg/kg, p.o.) attenuated PCP (10 mg/kg/day for 10 days)-induced cognitive deficits in mice, in a dose dependent manner. Furthermore, PCP (10 mg/kg)-induced cognitive deficits were also significantly ameliorated by subsequent subchronic (14 days) administration of the selective α1-adrenoceptor antagonist prazosin (1.0 mg/kg/day, ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949545</comments>
            <pubDate>Wed, 05 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949545</guid>        </item>
        <item>
            <title>Chronic treatment with 13-cis-retinoic acid changes aggressive behaviours in the resident–intruder paradigm in rats</title>
            <link>http://www.medworm.com/index.php?rid=2949547&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001692%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Retinoids, vitamin A related compounds, have an established role in the development of the nervous system and are increasingly recognized to play a role in adult brain function. The synthetic retinoid, 13-cis-retinoic acid (13-cis-RA, Roaccutane) is widely used to treat severe acne but has been linked to an increased risk of neuropsychiatric side effects, including depression. Here we report that chronic administration with 13-cis-RA (1mg/kg i.p. daily, 7–14days) in adult rats reduced aggression- and increased flight-related behaviours in the resident–intruder paradigm. However, in the forced swim, sucrose consumption and open field tests treatment for up to 6weeks with 13-cis-RA did not modify behaviour in adult or juvenile animals. The behavioural change observed in the res...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949547</comments>
            <pubDate>Mon, 03 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949547</guid>        </item>
        <item>
            <title>Epistasis between a set of variations located in the TAAR6 and HSP-70 genes toward schizophrenia and response to antipsychotic treatment</title>
            <link>http://www.medworm.com/index.php?rid=2860873&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001680%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Suggestive associations have been reported between trace amines and heat shock proteins, and a disrupted pathophysiology that enhances the risk of psychosis and that modifies responses to antipsychotic treatments. Our group previously reported genetic studies on TAAR6 and HSP-70 separately in patients with schizophrenia. In the current study, we investigated possible epistasis between the same set of variations in a sample of 281 patients diagnosed with schizophrenia and 288 healthy controls. We applied the generalized multifactor dimensionality reduction (MDR) method and controlled covariates significantly associated with both diagnosis and treatment efficacy. To the best of our knowledge, epistasis between the present set of variations in schizophrenia has not been tested befor...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860873</comments>
            <pubDate>Wed, 29 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860873</guid>        </item>
        <item>
            <title>Stress-mediated decreases in brain-derived neurotrophic factor as potential confounding factor for acute tryptophan depletion-induced neurochemical effects</title>
            <link>http://www.medworm.com/index.php?rid=2860874&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001667%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Acute tryptophan depletion (ATD) is extensively used to investigate the implication of serotonin (5-hydroxytryptamine; 5-HT) in the onset and treatment of depression and cognitive disorders. Brain-derived neurotrophic factor (BDNF) is strongly linked to the 5-HT system and plays an essential role in mood and memory processes. The present study investigated the effects of ATD upon BDNF in serum, hippocampus and prefrontal cortex in the rat to further explore the underlying mechanism of ATD.ATD significantly decreased peripheral tryptophan (TRP) levels and moderately interrupted 5-HT metabolism 4h after administration of the nutritional mixture. Although no direct effects of ATD upon serum or brain BDNF concentrations were found, a stress-mediated, decrease in BDNF was observed in ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860874</comments>
            <pubDate>Tue, 28 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860874</guid>        </item>
        <item>
            <title>Proapoptotic and chemosensitizing effects of selective serotonin reuptake inhibitors on T cell lymphoma/leukemia (Jurkat) in vitro</title>
            <link>http://www.medworm.com/index.php?rid=2746996&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001552%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: While selective serotonin reuptake inhibitors (SSRIs) are commonly used for psychiatric indications, evidence implies them to possess anti-cancerous properties as well. We evaluated such in vitro effects in malignant T cells (Jurkat), finding that exposure to high concentrations of sertraline (IC50=9.5µM) or paroxetine (IC50=18µM) yielded a considerable reduction in cellular viability, exceeding equimolar doses of the chemotherapeutics vincristine and cyclophosphamide (P (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746996</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746996</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2636742&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001801%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636742</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:35 +0100</pubDate>
            <guid isPermaLink="false">2636742</guid>        </item>
        <item>
            <title>ECNP Announcement: 2010 ECNP Workshop</title>
            <link>http://www.medworm.com/index.php?rid=2636741&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001813%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636741</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:35 +0100</pubDate>
            <guid isPermaLink="false">2636741</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2636740&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001783%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636740</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:35 +0100</pubDate>
            <guid isPermaLink="false">2636740</guid>        </item>
        <item>
            <title>Guide for Authors</title>
            <link>http://www.medworm.com/index.php?rid=2636739&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001898%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636739</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:35 +0100</pubDate>
            <guid isPermaLink="false">2636739</guid>        </item>
        <item>
            <title>Welcome message from the new editor</title>
            <link>http://www.medworm.com/index.php?rid=2636731&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001825%2Fabstract%3Frss%3Dyes</link>
            <description>Dear colleagues,  Traditionally, the foundations of medical education and progress have been paths of knowledge transfer — from master to trainee/apprentice, from colleague to colleague, and through the medical press, whose all-important task it is to gather the most recent and relevant scientific information, screen it for accuracy, and distribute it to the medical community. Over the last three decades, interrelated technological and social developments have changed the nature of medical education and the medical press, making the exchange of information virtually unlimited. European Neuropsychopharmacology is included in Thomson Reuters ISI Web of Knowledge in the categories clinical neurology, neurosciences, pharmacology &amp; pharmacy and psychiatry. Over 570 journals are being publishe...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636731</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:33 +0100</pubDate>
            <guid isPermaLink="false">2636731</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2636729&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001734%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636729</comments>
            <pubDate>Sat, 25 Jul 2009 11:29:33 +0100</pubDate>
            <guid isPermaLink="false">2636729</guid>        </item>
        <item>
            <title>Clomipramine treatment reversed the glial pathology in a chronic unpredictable stress-induced rat model of depression</title>
            <link>http://www.medworm.com/index.php?rid=2860872&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900162X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Growing evidence indicates that glia pathology contributes to the pathophysiology and possibly the etiology of depression. The study investigates changes in behaviors and glial fibrillary associated protein (GFAP) in the rat hippocampus after chronic unpredictable stress (CUS), a rat model of depression. Furthermore, we studied the effects of clomipramine, one of tricyclic antidepressants (TCAs), known to modulate serotonin and norepinephrine uptake, on CUS-induced depressive-like behaviors and GFAP levels. Rats exposed to CUS showed behavioral deficits in physical state, open field test and forced swimming test and exhibited a significant decrease in GFAP expression in the hippocampus. Interestingly, the behavioral and GFAP expression changes induced by CUS were reversed by chro...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860872</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860872</guid>        </item>
        <item>
            <title>Differential influence of selective 5-HT5A vs 5-HT1A, 5-HT1B, or 5-HT2C receptor blockade upon light-induced phase shifts in circadian activity rhythms: Interaction studies with citalopram</title>
            <link>http://www.medworm.com/index.php?rid=2949548&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001655%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, this is the first in vivo evidence for an influence of 5-HT5A receptors upon circadian rhythms, but no single class of 5-HT receptor mediates their control by citalopram. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949548</comments>
            <pubDate>Wed, 15 Jul 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949548</guid>        </item>
        <item>
            <title>Farewell message from the Founding Editors</title>
            <link>http://www.medworm.com/index.php?rid=2636730&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001679%2Fabstract%3Frss%3Dyes</link>
            <description>Twenty years have passed since the European College of Neuropsychopharmacology made the decision to found the College's journal; a bold and forward looking decision for an association that was very young at the time. Two editors were selected in order to focus on the publication of basic and of clinical research. We were honoured to be given the opportunity to watch over the birth of the journal and to contribute to its development. The members of ECNP represent a body of serious researchers working in a broad spectrum of disciplines and deserve a scientific journal of the first rank. Our editorial aims were clear: the journal should publish the most significant research papers and reviews in the field and become a journal of which the members could be proud. (Source: European Neuropsychop...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636730</comments>
            <pubDate>Tue, 14 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636730</guid>        </item>
        <item>
            <title>Brain opioid receptor binding in early abstinence from alcohol dependence and relationship to craving: An [11C]diprenorphine PET study</title>
            <link>http://www.medworm.com/index.php?rid=2746998&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900159X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The importance of the opioid receptor system in substance dependence is increasingly recognised. We used PET with the non-selective tracer [11C]diprenorphine to examine opioid receptor binding in early abstinence from alcohol dependence and the relationship to craving. We recruited 11 alcohol dependent patients and 13 controls. Subjects underwent one [11C]diprenorphine PET scan in early abstinence from dependent alcohol use (∼2weeks) and 2months later if continuously abstinent. Global and regional [11C]diprenorphine volumes of distribution (VD) were increased in alcohol dependent patients compared with controls but did not reach significance. We demonstrated a correlation between global and regional [11C]diprenorphine VD and craving in alcohol dependent patients which persisted...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746998</comments>
            <pubDate>Sun, 12 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746998</guid>        </item>
        <item>
            <title>Chronic fluoxetine differentially modulates the hippocampal microtubular and serotonergic system in grouped and isolation reared rats</title>
            <link>http://www.medworm.com/index.php?rid=2860870&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001576%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Social isolation from weaning in rats produces behavioural and hippocampal structural changes at adulthood. Here, rats were group or isolation reared for eight-weeks. Following the initial four-week period of rearing, fluoxetine (10mg/kg i.p.) was administered for 28days. Changes in recognition memory, hippocampal monoamines, and cytoskeletal microtubules were investigated. Isolation-rearing for four- or eight-weeks produced recognition memory deficits that were not reversed by fluoxetine. Eight-weeks of isolation decreased α-tubulin acetylation (Acet-Tub) and the tyrosinated/detyrosinated α-tubulin ratio (Tyr/Glu-Tub), suggesting major alterations in microtubule dynamics and neuronal plasticity. In grouped rats, fluoxetine decreased Acet-Tub without changes in Tyr/Glu-Tub. In ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860870</comments>
            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860870</guid>        </item>
        <item>
            <title>The antinociceptive properties of reboxetine in acute pain</title>
            <link>http://www.medworm.com/index.php?rid=2746997&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001564%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The antinociceptive effects of the selective noradrenaline reuptake inhibitor antidepressant reboxetine and its interaction with various opioid and noradrenaline receptor subtypes were evaluated. Reboxetine (i.p.) induced a weak dose-dependent antinociceptive effect in acute pain, using the hotplate model. The reboxetine-induced antinociception was significantly inhibited by the opioid receptor antagonists naloxone, nor-BNI, naltrindole and b-FNA, implying a non-selective role for the opioid receptors in the reboxetine's antinociceptive effect. The adrenergic antagonists yohimbine and phentolamine attenuated to some extent the reboxetine-induced antinociception, implying a minor adrenergic mechanism of antinociception. The addition of opioid or α2 agonists, did not potentiate th...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746997</comments>
            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746997</guid>        </item>
        <item>
            <title>Effect of basic fibroblast growth factor (FGF2) gene polymorphisms on SSRIs treatment response and side effects</title>
            <link>http://www.medworm.com/index.php?rid=2746995&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001588%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, this is the first study investigating the association of antidepressant response and intolerance with FGF2 variants. This finding adds an important piece of information for the pathway of detecting the genetics of antidepressant response. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746995</comments>
            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746995</guid>        </item>
        <item>
            <title>Altered expression and modulation of activity-regulated cytoskeletal associated protein (Arc) in serotonin transporter knockout rats</title>
            <link>http://www.medworm.com/index.php?rid=2949549&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001606%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A gene variant in the human serotonin transporter (SERT) can increase the vulnerability to mood disorders. SERT knockout animals show similarities to the human condition and represent an important tool to investigate the mechanisms underlying the pathologic condition in humans. Along this line of thinking, we used SERT KO rats (SERT+/− and SERT−/−) to investigate abnormalities in the expression and function of the activity-regulated gene Arc (Activity-regulated cytoskeletal associated protein) and the early inducible gene Zif-268, (zinc finger binding protein clone 268), which are important players in neuronal plasticity. We found lower basal Arc mRNA levels in hippocampus and prefrontal cortex of mutant rats in comparison with wild-type animals. Moreover SERT mutant rats s...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2949549</comments>
            <pubDate>Mon, 06 Jul 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2949549</guid>        </item>
        <item>
            <title>Response to prophylactic lithium in bipolar disorder may be associated with a preservation of executive cognitive functions</title>
            <link>http://www.medworm.com/index.php?rid=2860871&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001643%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We assessed performance on the Wisconsin Card Sorting Test (WCST), measuring executive functions, in 30 patients showing different prophylactic effect of lithium (excellent lithium responders—ER, partial responders—PR and non-responders—NR), and in fifty persons of their offspring (12 of ER, 26 of PR, and 12 of NR). Age- and gender head-to-head matched population consisted of 30 subjects for lithium group and 50 subjects for the offspring of lithium patients. In lithium patients, NR had significantly worse results compared to the remaining groups and to control subjects on perseverative errors (WCST-P) and conceptual responses (WCST-%conc). No differences were observed in the offspring of patients with different effect of lithium, however, they showed an impairment on WCST-...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860871</comments>
            <pubDate>Sun, 05 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860871</guid>        </item>
        <item>
            <title>A novel compound N1,N5-(Z)-N10-(E)-tri-p-coumaroylspermidine isolated from Carthamus tinctorius L. and acting by serotonin transporter inhibition</title>
            <link>http://www.medworm.com/index.php?rid=2746999&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001618%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Safflower, the dry flower of Carthamus tinctorius L., has long been applied for empirically treating cerebral ischemia and depression in traditional Chinese medicine. Pathogenesis of major depression involves monoaminergic transmission. The present study assessed whether safflower or its isolate would be effective in functionally regulating monoamine transporter using in vitro screening cell lines. We discovered that safflower insoluble fraction significantly inhibited serotonin uptake in Chinese hamster ovary cells stably expressing serotonin transporter (i.e. S6 cells). This fraction went through an activity-guided isolation and an active ingredient was obtained, which was subsequently elucidated as a novel coumaroylspermidine analog N1,N5-(Z)-N10-(E)-tri-p-coumaroylspermidine ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746999</comments>
            <pubDate>Sun, 05 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746999</guid>        </item>
        <item>
            <title>Frontal EEG predictors of treatment outcome in major depressive disorder</title>
            <link>http://www.medworm.com/index.php?rid=2860869&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001631%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Using automated analysis of frontal EEG collected during the first week of antidepressant treatment it may be possible to facilitate prediction of SSRI or venlafaxine efficacy in MDD. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860869</comments>
            <pubDate>Thu, 02 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860869</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2519950&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001515%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519950</comments>
            <pubDate>Fri, 26 Jun 2009 14:50:04 +0100</pubDate>
            <guid isPermaLink="false">2519950</guid>        </item>
        <item>
            <title>Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2519949&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001497%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519949</comments>
            <pubDate>Fri, 26 Jun 2009 14:50:04 +0100</pubDate>
            <guid isPermaLink="false">2519949</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2519940&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001448%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519940</comments>
            <pubDate>Fri, 26 Jun 2009 14:50:04 +0100</pubDate>
            <guid isPermaLink="false">2519940</guid>        </item>
        <item>
            <title>SSRIs, bone mineral density, and risk of fractures — a review</title>
            <link>http://www.medworm.com/index.php?rid=2746991&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001424%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A possibility for selective serotonin reuptake inhibitors (SSRIs) to increase the risk of bone fracture has been debated during recent years. Proposed causes include an ability for the drugs to reduce bone mineral density (BMD). Experimental data have identified a functional 5-HT system in bone, although its role is unclear. Results from numerous epidemiological studies are heterogeneous and several different associations have been suggested; between depression and low BMD, SSRIs and low BMD, depression and falls, SSRIs and falls, depression and fractures, and SSRIs and fractures. In this paper, we review the available data and discuss the various study results. Based on the current available data, we conclude that it is not possible to determine whether SSRIs may negatively infl...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746991</comments>
            <pubDate>Sun, 21 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746991</guid>        </item>
        <item>
            <title>Prenatal viral infection of mice at E16 causes changes in gene expression in hippocampi of the offspring</title>
            <link>http://www.medworm.com/index.php?rid=2636735&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000911%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The hippocampus governs memory formation and emotional regulation, and there is widespread evidence of hippocampal dysfunction in psychiatric disorders, including schizophrenia and autism. There is abundant evidence that prenatal viral infection may play a role in the development of these two disorders. In the current study, we have examined gene expression and structural changes of the hippocampi of exposed neonates following maternal infection at embryonic day (E) 16 (middle second trimester). We observed significant changes in gene expression in the offspring at postnatal day (P) 0 (birth), P14 (childhood), and P56 (adulthood), including a number of candidate genes for autism and schizophrenia. qRT-PCR verified the direction and magnitude of change for 5 of the genes from the ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636735</comments>
            <pubDate>Sun, 07 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636735</guid>        </item>
        <item>
            <title>Molecular tools for assessing human depression by positron emission tomography</title>
            <link>http://www.medworm.com/index.php?rid=2636732&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000996%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We review reports published over the past 5 years on positron emission tomography (PET) of neurotransmission in depressive disorders. The molecular tools of PET neuroimaging are compounds labeled with a positron-emitting nuclide. PET radioligands have been used in recent years to study several aspects of monoaminergic and cholinergic neurotransmission in the brain of depressed subjects and healthy controls. The value of kinetic parameters of certain PET radioligands has often been reported to be lower in depressed subjects than in healthy ones, but there is usually no reliable relationship between the binding potential of the neuroreceptor or transporter and the clinical condition of depressed subject. In addition, many recent PET studies have noted either higher binding potenti...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636732</comments>
            <pubDate>Sun, 07 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636732</guid>        </item>
        <item>
            <title>Tolerability of outpatient antipsychotic treatment: 36-month results from the European Schizophrenia Outpatient Health Outcomes (SOHO) study</title>
            <link>http://www.medworm.com/index.php?rid=2519942&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000893%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, antipsychotics have different tolerability profiles in terms of the adverse events we monitored. Results should be interpreted conservatively due to the observational study design. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519942</comments>
            <pubDate>Sun, 07 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519942</guid>        </item>
        <item>
            <title>Association between corneal temperature and mental status of treatment-resistant schizophrenia inpatients</title>
            <link>http://www.medworm.com/index.php?rid=2636736&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001199%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: This study indicates that treatment-resistant overtly psychotic schizophrenia inpatients' mental status (as assessed by the PANSS) correlates with their corneal temperature. The relevance of these phenomena to the pathophysiology of schizophrenia, the biological mechanism underlying corneal temperature alterations and the possible role of temperature-modulating drugs (neuroleptics or non-neuroleptics) on schizophrenic psychosis merits further large-scale investigation in both medicated- and drug-free schizophrenia patients compared to matched controls. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636736</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636736</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2444959&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001308%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2444959</comments>
            <pubDate>Sat, 30 May 2009 22:28:43 +0100</pubDate>
            <guid isPermaLink="false">2444959</guid>        </item>
        <item>
            <title>ECNP Announcement: Deadline Late Registration - 22nd ECNP Congress</title>
            <link>http://www.medworm.com/index.php?rid=2444958&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900131X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2444958</comments>
            <pubDate>Sat, 30 May 2009 22:28:43 +0100</pubDate>
            <guid isPermaLink="false">2444958</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2444957&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900128X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2444957</comments>
            <pubDate>Sat, 30 May 2009 22:28:43 +0100</pubDate>
            <guid isPermaLink="false">2444957</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2444956&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001230%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2444956</comments>
            <pubDate>Sat, 30 May 2009 22:28:43 +0100</pubDate>
            <guid isPermaLink="false">2444956</guid>        </item>
        <item>
            <title>A distinct pattern of intracellular glucocorticoid-related responses is associated with extreme behavioral response to stress in an animal model of post-traumatic stress disorder</title>
            <link>http://www.medworm.com/index.php?rid=2860868&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001187%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Following the uniform acute response, the patterns of GR protein levels and Zif/268 mRNA levels are associated with degree of behavioral disruption. Since the slower-onset mechanism for glucocorticoid-induced Zif/268 expression depends on activation of the MAPK pathway, the pattern observed only in EBR rats may be related to disruptions of this pathway. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2860868</comments>
            <pubDate>Sun, 24 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2860868</guid>        </item>
        <item>
            <title>Antipsychotics in children and adolescents: Increasing use, evidence for efficacy and safety concerns</title>
            <link>http://www.medworm.com/index.php?rid=2636733&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001217%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Second-generation antipsychotics (SGA) are increasingly used to treat children and adolescents. The European College of Neuro-psychopharmacology convened an expert panel to review relevant efficacy and safety data, and identify needs for further research. Controlled studies support the short-term efficacy of several SGA for treating psychosis, mania, and aggression within certain diagnostic categories. Except for clozapine, no clinically significant superiority in efficacy has been demonstrated for any specific antipsychotic, including both first- and second-generation agents, in children and adolescents. Major differences exist, however, with respect to type and severity of adverse effects; therefore the choice of treatment is primarily guided by tolerability and safety consider...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636733</comments>
            <pubDate>Sun, 24 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636733</guid>        </item>
        <item>
            <title>Sertindole causes distinct electrocardiographic T-wave morphology changes</title>
            <link>http://www.medworm.com/index.php?rid=2746993&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001205%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Sertindole's propensity to prolong the QT interval relates to blockade of the KCNH2 (HERG) encoded Ikr potassium channel, but there has been limited detailed data on T-wave morphology changes. Digital 12-lead ECG was recorded at baseline and at steady-state in 37 patients switched to sertindole. ECG was analyzed for quantitative T-wave morphology changes and Fridericia-corrected QT duration (QTcF). Prominent T-wave morphology changes occurred during sertindole treatment and in some cases without concomitant prolongation of the QTcF interval. Four patients developed notched T-waves during sertindole treatment. Mean QTc prolongation was 19 ms. The mean effect size was higher for T-wave morphology combination score (MCS) (ES=1.92; 95% CI: 1.35–2.49) compared to the mean effect si...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746993</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746993</guid>        </item>
        <item>
            <title>Immediate versus gradual suspension of previous treatments during switch to aripiprazole: Results of a randomized, open label study</title>
            <link>http://www.medworm.com/index.php?rid=2519944&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000959%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The aim of the present work was to investigate possible differences in terms of efficacy and tolerability between different switching options to aripiprazole. 77 subjects were randomly assigned to (1) administration of aripiprazole (10 mg) with simultaneous discontinuation of current antipsychotic; (2) administration of aripiprazole (10 mg) and tapering off current antipsychotic over 4 weeks with half dose after the first 2 weeks; (3) administration of aripiprazole (10 mg) and tapering off current antipsychotic over 6 weeks with half dose after the first 2 weeks. Efficacy assessments included CGI-S, CGI-I, BPRS and SANS. Safety assessments included SAS, BAS and AIMS. Severity of symptoms significantly decreased from baseline over the 12 weeks of treatment. Patients switch...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519944</comments>
            <pubDate>Tue, 12 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519944</guid>        </item>
        <item>
            <title>Conditioned place preference induced by social play behavior: Parametrics, extinction, reinstatement and disruption by methylphenidate</title>
            <link>http://www.medworm.com/index.php?rid=2636737&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000935%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated behavioral factors underlying conditioned place preference (CPP) induced by social interaction in adolescent rats. We found that the magnitude of socially-induced CPP depended on the social motivation of the animals and on the amount of training. After extinction, socially-induced CPP could be reinstated by a single reconditioning session. Treatment with methylphenidate, which disrupts social play behavior in adolescent rats, but not social exploratory behavior, prevented the development of socially-induced CPP. Interestingly, methylphenidate by itself induced CPP. These data demonstrate that: 1. social interaction is rewarding in adolescent rats; 2. appetitive and mnemonic factors influence the development of socially-induced CPP; 3. comparable to drug-induc...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636737</comments>
            <pubDate>Mon, 11 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636737</guid>        </item>
        <item>
            <title>Psychopharmacology for children: From off label use to registration</title>
            <link>http://www.medworm.com/index.php?rid=2519948&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001175%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Pharmacological treatment of children and adolescents is largely based on evidence from adults' studies. There is, however, growing awareness that this evidence cannot simply be extrapolated to children. The Dutch Medicines Evaluation Board (MEB) in collaboration with the Child and Adolescent section of the Dutch Association of Psychiatry and the National Expertise Centre Child and Adolescent Psychiatry have organised a workshop to discuss the kind of evidence that would be necessary and the methods involved. There was consensus about the need to demonstrate efficacy in targeted disorders as well as symptoms within specific disorders and about the need for separate evidence for children and for adolescents. In addition, too little is known about safety, especially long-term safet...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519948</comments>
            <pubDate>Mon, 11 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519948</guid>        </item>
        <item>
            <title>Characteristics and consequences of muscarinic receptor activation by tau protein</title>
            <link>http://www.medworm.com/index.php?rid=2746994&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900100X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: It was recently suggested that tau protein released as a result of neuronal death is toxic to neighbouring cells, an effect that is mediated through the activation of muscarinic M1 and/or M3 receptors. Nevertheless, why tau protein and not other native muscarinic agonists, like ACh, can induce this neurotoxicity remains unknown. To clarify this issue, we analysed the different responses and properties of muscarinic receptors in response to stimulation by tau or ACh. The results revealed that the tau protein has an affinity for muscarinic receptors of around one order of magnitude higher than that of ACh. Furthermore, while the repeated stimulation with ACh induces desensitization of the muscarinic receptors, reiterate stimulation with tau failed to produce this phenomenon. Finall...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746994</comments>
            <pubDate>Thu, 07 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746994</guid>        </item>
        <item>
            <title>Pindolol augmentation enhances response outcomes in first depressive episodes</title>
            <link>http://www.medworm.com/index.php?rid=2495096&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000984%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Effectiveness of Pindolol addition to SSRIs is still a matter of debate. Recently, Geretsegger et al. [Geretsegger, C., Bitterlich, W., Stelzig, R., Stuppaeck, C., Bondy, B. and Aichhorn, W. (2008) Paroxetine with Pindolol augmentation: a double-blind, randomized, placebo-controlled study in depressed in-patients. Eur. Neuropsychopharmacol. 18, 141–146.] have found that never-medicated depressed patients showed a significant sustained response with Paroxetine + Pindolol treatment. Also, patients with a first depressive episode displayed a trend for higher sustained response rates with Pindolol co-administration. Re-analysing the data of a previous clinical trial of Fluoxetine + Pindolol [Pérez, V., Gilaberte, I., Faries, D., Alvarez, E. and Artigas, F. (1997). Randomised, doub...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495096</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495096</guid>        </item>
        <item>
            <title>Advantages and disadvantages of combination treatment with antipsychotics: ECNP Consensus Meeting, March 2008, Nice</title>
            <link>http://www.medworm.com/index.php?rid=2495097&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000972%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Terminology and principles of combining antipsychotics with a second medication: The term “combination” includes virtually all the ways in which one medication may be added to another. The other commonly used terms are “augmentation” which implies an additive effect from adding a second medicine to that obtained from prescribing a first, an “add on” which implies adding on to existing, possibly effective treatment which, for one reason or another, cannot or should not be stopped. The issues that arise in all potential indications are: a) how long it is reasonable to wait to prove insufficiency of response to monotherapy; b) by what criteria that response should be defined; c) how optimal is the dose of the first monotherapy and, therefore, how confident can one be tha...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495097</comments>
            <pubDate>Mon, 04 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495097</guid>        </item>
        <item>
            <title>Documented poor sleep among methadone-maintained patients is associated with chronic pain and benzodiazepine abuse, but not with methadone dose</title>
            <link>http://www.medworm.com/index.php?rid=2519946&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000960%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Patients with chronic pain or BDZ abuse presented both perceived and objective poorer sleep, regardless of methadone dosage. Sleep evaluation and treatment should address these two prevalent conditions in order to improve MMT patients' quality of sleep (and of life) and overall treatment outcome. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519946</comments>
            <pubDate>Sun, 03 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519946</guid>        </item>
        <item>
            <title>Modulation of the Ca2+ conductance of nicotinic acetylcholine receptors by Lypd6</title>
            <link>http://www.medworm.com/index.php?rid=2636738&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000947%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The agonist binding sensitivity and desensitization kinetics of nicotinic acetylcholine receptors (nAChRs) can be modulated by snake venom neurotoxins and related endogenous small proteins of the uPAR-Ly6 family. Here we identify Lypd6, a distantly related member of the u-PAR/Ly-6 family expressed in neurons as a novel modulator of nAChRs. Lypd6 overexpressed in trigeminal ganglia neurons selectively enhanced the Ca2+-component of nicotine-evoked currents through nAChRs, as evidenced by comparative whole-cell patch clamp recordings and Ca2+-imaging in wildtype and transgenic mice overexpressing Lypd6. In contrast, a knockdown of Lypd6 expression using siRNAs selectively reduced nicotine-evoked Ca2+-currents. Pharmacological experiments revealed that the nAChRs involved in this pr...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636738</comments>
            <pubDate>Wed, 29 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636738</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2372269&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001096%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372269</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:24 +0100</pubDate>
            <guid isPermaLink="false">2372269</guid>        </item>
        <item>
            <title>Call for Breaking News</title>
            <link>http://www.medworm.com/index.php?rid=2372268&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001102%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372268</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:24 +0100</pubDate>
            <guid isPermaLink="false">2372268</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2372267&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001072%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372267</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:24 +0100</pubDate>
            <guid isPermaLink="false">2372267</guid>        </item>
        <item>
            <title>Serotonin transporter promoter region polymorphisms do not influence treatment response to escitalopram in patients with major depression</title>
            <link>http://www.medworm.com/index.php?rid=2372266&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000339%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we investigated the impact of 5-HTTLPR and a functional SNP rs25531 on the treatment outcomes to escitalopram in depressive patients. The study sample consisted of 135 outpatients with major depressive disorder (mean age 31.1±11.6 years, 68% females) treated with escitalopram 10–20 mg/day for 12 weeks. There were no significant associations between 5-HTT promoter region polymorphisms and response rate or mean change of depressive symptoms during escitalopram treatment. However we showed that patients carrying S allele of 5-HTTLPR may have increased risk for some side effects, including headache, induced by escitalopram medication. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372266</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:23 +0100</pubDate>
            <guid isPermaLink="false">2372266</guid>        </item>
        <item>
            <title>D1-like receptor activation improves PCP-induced cognitive deficits in animal models: Implications for mechanisms of improved cognitive function in schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=2372265&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000303%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Phencyclidine (PCP) produces cognitive deficits of relevance to schizophrenia in animal models. The aim was to investigate the efficacy of the D1-like receptor agonist, SKF-38393, to improve PCP-induced deficits in the novel object recognition (NOR) and operant reversal learning (RL) tasks. Rats received either sub-chronic PCP (2 mg/kg) or vehicle for 7 days, followed by a 7-day washout. Rats were either tested in NOR or the RL tasks. In NOR, vehicle rats successfully discriminated between novel and familiar objects, an effect abolished in PCP-treated rats. SKF-38393 (6 mg/kg) significantly ameliorated the PCP-induced deficit (P (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372265</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:22 +0100</pubDate>
            <guid isPermaLink="false">2372265</guid>        </item>
        <item>
            <title>The partial 5-HT1A receptor agonist buspirone enhances neurogenesis in the opossum (Monodelphis domestica)</title>
            <link>http://www.medworm.com/index.php?rid=2372264&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000273%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We demonstrate for the first time that neurogenesis in the adult Monodelphis opossum has a typical mammalian pattern and occurs only in the dentate gyrus (DG) and subventricular zone (SVZ) of the lateral ventricles. In these two brain regions neurogenesis is present throughout the lifespan, although its rate is reduced by half in the old age. Treatment with buspirone, a partial 5-HT1A receptor agonist which is used in human clinic as an anxiolytic agent, boosts proliferation in the SVZ and DG in both adult and aged opossums. The neuronal phenotype dominates among newly generated cells in both non-treated and buspirone-treated opossums. We suggest that if functional importance of adult neurogenesis is in improving olfactory discrimination and generation of hippocampus-dependent me...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372264</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:20 +0100</pubDate>
            <guid isPermaLink="false">2372264</guid>        </item>
        <item>
            <title>Effects of the dopamine stabilizer, OSU-6162, on brain stimulation reward and on quinpirole-induced changes in reward and locomotion</title>
            <link>http://www.medworm.com/index.php?rid=2372263&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000261%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the effects of several doses of OSU-6162, a drug that belongs to a new class named “DA stabilizers”, on brain stimulation reward. Because quinpirole produces, depending on the dose, a pre-synaptic depressant and a post-synaptic stimulatory effect on reward and locomotor activity, we also compared the ability of OSU-6162 and haloperidol to prevent these effects of the full DA agonist. Results show that OSU-6162 produced a dose-orderly reduction of reward with no change in the capacity of the animals to produce the operant response, and prevented, like haloperidol, both stimulatory and depressant effects of quinpirole on locomotor activity but only its reward stimulatory effect. The observed functional antagonism of OSU-6162 on these DA-dependent behaviors ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372263</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:14 +0100</pubDate>
            <guid isPermaLink="false">2372263</guid>        </item>
        <item>
            <title>The influence of psychiatric comorbidity on the dexamethasone/CRH test in major depression</title>
            <link>http://www.medworm.com/index.php?rid=2372262&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000686%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: An enhanced suppression of cortisol to 1.5 mg DEX is present in a subgroup of depressed patients with psychiatric comorbidity. Distinct hypothalamic-pituitary-adrenal (HPA) axis dysfunctions are revealed when comorbidity is taken into account. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372262</comments>
            <pubDate>Wed, 29 Apr 2009 04:14:06 +0100</pubDate>
            <guid isPermaLink="false">2372262</guid>        </item>
        <item>
            <title>Repeated stress prevents cocaine-induced activation of BDNF signaling in rat prefrontal cortex</title>
            <link>http://www.medworm.com/index.php?rid=2372261&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900011X%2Fabstract%3Frss%3Dyes</link>
            <description>In this report we provide evidence that repeated stress prevents cocaine-induced activation of BDNF expression and signaling in rat prefrontal cortex. A single injection of cocaine up-regulates BDNF expression in sham (i.e. unstressed) rats but not in repeatedly stressed rats. Similarly, the expression as well as trafficking of the high affinity BDNF receptor trkB promoted by the psychostimulant is impaired in chronically-stressed rats challenged with cocaine.Moreover, among the different intracellular signaling pathways that can be activated by the neurotrophin, i.e. ERK1/2-, Akt- and PLCγ-pathway, we found that cocaine is able to selectively activate the ERK1/2 pathway in sham animals, but not in rats exposed to repeated stress. Notably, such changes take place in chronically-stressed a...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372261</comments>
            <pubDate>Wed, 29 Apr 2009 04:13:54 +0100</pubDate>
            <guid isPermaLink="false">2372261</guid>        </item>
        <item>
            <title>An epigenetic intervention interacts with genetic strain differences to modulate the stress-induced reduction of flurazepam's antiseizure efficacy in the mouse</title>
            <link>http://www.medworm.com/index.php?rid=2372260&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000078%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Stress induces changes in the endogenous tone of both GABA and NMDA receptor-mediated neurotransmission in the intact mouse. Because changes are observed 24 h after stress, epigenetically-regulated alterations in gene expression may mediate these effects. In earlier work, sodium butyrate, a centrally-active histone deacetylase inhibitor that promotes gene expression, was shown to modulate the stress-induced reduction of the ability of MK-801 (dizocilpine), a noncompetitive NMDA receptor antagonist, to antagonize electrically-precipitated seizures. In the current study, we extended this work to look at sodium butyrate's modulatory effect on stress-induced changes in the antiseizure efficacy of flurazepam, a benzodiazepine receptor agonist, in two strains of mice. Epigenetic mecha...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372260</comments>
            <pubDate>Wed, 29 Apr 2009 04:13:48 +0100</pubDate>
            <guid isPermaLink="false">2372260</guid>        </item>
        <item>
            <title>MDMA reinstates cocaine-seeking behaviour in mice</title>
            <link>http://www.medworm.com/index.php?rid=2372259&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000066%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions:: Acute MDMA can reinstate cocaine-seeking behaviour in mice. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372259</comments>
            <pubDate>Wed, 29 Apr 2009 04:13:40 +0100</pubDate>
            <guid isPermaLink="false">2372259</guid>        </item>
        <item>
            <title>Research in anxiety disorders: From the bench to the bedside</title>
            <link>http://www.medworm.com/index.php?rid=2372258&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000340%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The development of ethologically based behavioural animal models has clarified the anxiolytic properties of a range of neurotransmitter and neuropeptide receptor agonists and antagonists, with several models predicting efficacy in human clinical samples.Neuro-cognitive models of human anxiety and findings from fMRI suggest dysfunction in amygdala-prefrontal circuitry underlies biases in emotion activation and regulation. Cognitive and neural mechanisms involved in emotion processing can be manipulated pharmacologically, and research continues to identify genetic polymorphisms and interactions with environmental risk factors that co-vary with anxiety-related behaviour and neuro-cognitive endophenotypes.This paper describes findings from a range of research strategies in anxiety, d...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372258</comments>
            <pubDate>Wed, 29 Apr 2009 04:13:29 +0100</pubDate>
            <guid isPermaLink="false">2372258</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2372257&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09001023%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2372257</comments>
            <pubDate>Wed, 29 Apr 2009 04:13:28 +0100</pubDate>
            <guid isPermaLink="false">2372257</guid>        </item>
        <item>
            <title>Modulation of sickness behavior by sleep: The role of neurochemical and neuroinflammatory pathways in mice</title>
            <link>http://www.medworm.com/index.php?rid=2519947&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000923%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Activation of the immune system elicits several behavioral changes that are collectively called sickness behavior and consists in a strategy to overcome infection. Sleep deprivation can increase susceptibility to pathogens and to behavioral alterations. Thus, the present study aimed to determine how paradoxical sleep deprivation (PSD) affects the behavioral and neurochemical responses to lipopolysaccharide (LPS, potent activator of the immune response). Adult inbred mice were paradoxical sleep deprived (72 h), whereas the control group was kept in their home cages. Both groups received either an injection of saline or LPS (5, 10 or 20 µg/animal ip) before behavioral tasks and tissue collection. During the recovery sleep period, LPS provoked a strong inhibition of sleep rebound...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519947</comments>
            <pubDate>Sun, 26 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519947</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2344725&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000777%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344725</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:13 +0100</pubDate>
            <guid isPermaLink="false">2344725</guid>        </item>
        <item>
            <title>ECNP Announcement: ECNP Incentives - Young Scientists</title>
            <link>http://www.medworm.com/index.php?rid=2344724&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000789%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344724</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:13 +0100</pubDate>
            <guid isPermaLink="false">2344724</guid>        </item>
        <item>
            <title>ECNP Calendar of Events</title>
            <link>http://www.medworm.com/index.php?rid=2344723&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000753%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344723</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:13 +0100</pubDate>
            <guid isPermaLink="false">2344723</guid>        </item>
        <item>
            <title>The effects of synthetic and endogenous imidazoline binding site ligands on neuronal activity in discrete brain regions of naive and restraint-stressed rats</title>
            <link>http://www.medworm.com/index.php?rid=2344722&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000108%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We have mapped Fos expression to investigate brain regions activated by synthetic selective I2 (BU224) and endogenous (harmane) imidazoline binding site ligands in naive and restraint-stressed rats. Systemic administration of BU224 or harmane to naive rats increased Fos-like immunoreactivity (FLI) in the hypothalamic paraventricular nucleus (PVN), hippocampal dentate gyrus (DG), central and medial nuclei of the amygdala (CeA, MeA) and the locus coeruleus (LC). FLI in restraint-stressed rats was increased in all 5 regions by harmane, and in the CeA, MeA and LC by BU224. Dual-labelling of FLI cells in the PVN of naive rats showed an increase in the number of corticotrophin-releasing-factor-containing cells (CRF) activated by BU224 and harmane. Several CRF-containing neurons in the ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344722</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:10 +0100</pubDate>
            <guid isPermaLink="false">2344722</guid>        </item>
        <item>
            <title>MAO-A and COMT genotypes as possible regulators of perinatal serotonergic symptoms after in utero exposure to SSRIs</title>
            <link>http://www.medworm.com/index.php?rid=2344721&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000133%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Intrauterine exposure to SSRIs in late pregnancy can cause various serotonergic symptoms in the newborns. We associated the severity of these symptoms to neurotransmitter concentrations and genetic polymorphisms in the cytochrome P450, MAO-A and COMT enzymes. Altogether 20 children with prenatal exposure to citalopram or fluoxetine were genotyped. Infants with two high-activity alleles of the MAO-A gene had significantly higher serotonergic symptom scores than infants with at least one low-activity allele (mean 8.8 vs. 2.4, p=0.024). These infants had also higher cord blood DHPG concentrations (p=0.0054). Carriers of the high-activity COMT alleles had higher cord blood prolactin concentrations (p=0.044). According to our results, the higher serotonergic symptom score and cord blo...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344721</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:09 +0100</pubDate>
            <guid isPermaLink="false">2344721</guid>        </item>
        <item>
            <title>Differential effects of aripiprazole and haloperidol on BDNF-mediated signal changes in SH-SY5Y cells</title>
            <link>http://www.medworm.com/index.php?rid=2344720&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000054%2Fabstract%3Frss%3Dyes</link>
            <description>We examined the effects of aripiprazole (five and 10 μM) and haloperidol (one and 10 μM) on BDNF gene promoter activity in SH-SY5Y cells transfected with a rat BDNF promoter fragment (−108 to +340) linked to the luciferase reporter gene. The changes in BDNF, p-GSK-3β, and Bcl-2 levels were measured by Western blot analysis. The haloperidol was not associated with a significant difference in BDNF promoter activity. In contrast, aripiprazole was associated with increased BDNF promoter activity only with a dose of 10 μM (93%, p (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344720</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:07 +0100</pubDate>
            <guid isPermaLink="false">2344720</guid>        </item>
        <item>
            <title>Plasma Brain-Derived Neurotrophic Factor in treatment-resistant depressed patients receiving electroconvulsive therapy</title>
            <link>http://www.medworm.com/index.php?rid=2344719&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000091%2Fabstract%3Frss%3Dyes</link>
            <description>This study aimed to investigate whether the clinical course of medication-resistant depressed patients following a course of ECT might be associated with changes of plasma BDNF concentrations. Our findings showed that at T0 (baseline) plasma BDNF levels of patients were significantly lower than those of control subjects, and that at T2 (after ECT) were significantly increased in parallel with the decrease of the Hamilton Rating Scale for Depression (HRSD) total score. However, only remitter patients who showed higher baseline BDNF levels than non-remitters reached normalized BDNF levels after ECT. These findings would suggest the potential usefulness of baseline plasma BDNF levels as predictors of response to ECT in treatment-resistant depressed patients. (Source: European Neuropsychopharm...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344719</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:07 +0100</pubDate>
            <guid isPermaLink="false">2344719</guid>        </item>
        <item>
            <title>Behavioral changes in G72/G30 transgenic mice</title>
            <link>http://www.medworm.com/index.php?rid=2344718&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000042%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Genetic studies have implicated the evolutionary novel, primates-specific gene locus G72/G30 in schizophrenia, bipolar and panic disorders. It encodes for a protein LG72 whose function has been controversially discussed as putative regulator of the peroxisomal enzyme D-amino-acid-oxidase (DAO), or as a mitochondrial protein, which promotes robust mitochondrial fragmentation in mammalian cell lines including human and rat primary neurons. Because of this conserved function we here have generated “humanized” BAC transgenic mice (G72Tg) expressing alternatively spliced G72 and G30 transcripts, and the LG72 protein. G72 expression is prominent in granular cells of the cerebellum, the hippocampus, the cortex and the olfactory bulb. Most strikingly, G72Tg mice displayed deficits in...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344718</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:01 +0100</pubDate>
            <guid isPermaLink="false">2344718</guid>        </item>
        <item>
            <title>Repeated electroconvulsive seizures increase the total number of synapses in adult male rat hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=2344717&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000030%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The underlying mechanism of the therapeutic effect of electroconvulsive therapy (ECT) is still unclear. Here we investigated whether repeated electroconvulsive seizures (ECS), an animal model of ECT, in rats induce neuroplastic changes in the subregions of the hippocampus. ECS or sham treatment was given daily for 10 days to adult male rats. Stereological principles were employed to quantify volumes and the number of neurons and synapses. Volumes of granule cell layer (GCL) and Hilus in Dentate Gyrus of the hippocampus were significantly larger in the ECS treatment group. The neuron numbers in GCL, synapse numbers (including total synapses, spine synapses, and both perforated and nonperforated spine synapse subtypes) and synapse height in CA1 were significantly increased in the ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344717</comments>
            <pubDate>Mon, 20 Apr 2009 18:29:00 +0100</pubDate>
            <guid isPermaLink="false">2344717</guid>        </item>
        <item>
            <title>Genetic study of BDNF, DRD3, and their interaction in tardive dyskinesia</title>
            <link>http://www.medworm.com/index.php?rid=2344716&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900008X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Tardive dyskinesia (TD) is a neuroleptic-induced movement disorder. Its pathophysiology is unclear. The most consistent genetic findings have shown an association with the Ser9Gly polymorphism of the DRD3 gene. However, only few polymorphisms within DRD3 has been tested, and a comprehensive examination of DRD3 in TD is still lacking. Further, brain-derived neurotrophic factor (BDNF), a neuronal growth and survival peptide, regulates DRD3 expression and may be involved in the neuronal degeneration observed in TD. In the present study, we investigated 15 tag DRD3 polymorphisms and four tag BDNF polymorphisms for association with TD in our sample of Caucasian schizophrenia patients (N=171). While BDNF markers showed no association, a haplotype containing rs3732782, rs905568, and rs7...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344716</comments>
            <pubDate>Mon, 20 Apr 2009 18:28:59 +0100</pubDate>
            <guid isPermaLink="false">2344716</guid>        </item>
        <item>
            <title>Dopamine and serotonin release in the nucleus accumbens during starvation-induced hyperactivity</title>
            <link>http://www.medworm.com/index.php?rid=2344715&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000029%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Activity-based anorexia (ABA) is considered an animal model for anorexia nervosa (AN). By scheduled feeding and voluntary wheel running, it mimics severe body weight loss and increased physical activity in AN. Pharmacological, genetic and imaging studies implicate dopamine and serotonin in the regulation of feeding behavior, food-anticipatory activity, and food reward. Previous studies propose that the nucleus accumbens (NAc) plays an important role in these food-related processes. Here we determined dopamine and serotonin levels in the NAc upon exposure to the ABA model. Surprisingly, the release of dopamine and serotonin in the NAc were not increased during the initiation of food-anticipatory behavior in ABA rats. Dopamine release in the NAc was increased during feeding behavio...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344715</comments>
            <pubDate>Mon, 20 Apr 2009 18:28:58 +0100</pubDate>
            <guid isPermaLink="false">2344715</guid>        </item>
        <item>
            <title>Committee for Medicinal Products for Human Use (CHMP) assessment on efficacy of antidepressants</title>
            <link>http://www.medworm.com/index.php?rid=2344714&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000315%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The CHMP concluded that the approval of antidepressants for the treatment of patients with major depression is based on data that provide robust and sufficient evidence of clinically meaningful benefits for patients with major depression. Therefore, the CHMP is of the opinion that, as no public health concerns have been identified, no regulatory action is necessary on the basis of Kirsch et al.'s findings. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344714</comments>
            <pubDate>Mon, 20 Apr 2009 18:28:57 +0100</pubDate>
            <guid isPermaLink="false">2344714</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2344713&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000704%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2344713</comments>
            <pubDate>Mon, 20 Apr 2009 18:28:57 +0100</pubDate>
            <guid isPermaLink="false">2344713</guid>        </item>
        <item>
            <title>Increased use of antibiotics in patients treated with clozapine</title>
            <link>http://www.medworm.com/index.php?rid=2495092&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000881%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Clozapine has the potential to cause agranulocytosis and an association to an increased risk of infections has been suggested. Patients with an ICD-10 F20.x were identified from the Danish Central Psychiatric Research Registry and were linked to the national prescription database to identify schizophrenia patients treated with clozapine from 1996 to 2005(N=3374). Binomial regression and Cox proportional hazards models were used. An increased use of antibiotics was found RR=1.43, CI: 1.26–1.61, P (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495092</comments>
            <pubDate>Tue, 07 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495092</guid>        </item>
        <item>
            <title>DHEA and DHEA-S levels in hospitalized adolescents with first-episode schizophrenia and conduct disorder: A comparison study</title>
            <link>http://www.medworm.com/index.php?rid=2495094&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X0900090X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Introduction: Increasing evidence exists indicating an association of DHEA and DHEA-S blood levels with psychosis, however many of the findings remain contradictory based on different phases of the illness, different treatments and at a range of ages. To date no studies exist investigating the levels of these neurosteroids in adolescents with psychosis. Such an investigation would be important in order to exclude effects of chronic illness, long-term treatment and repeated hospitalizations.Method: Peripheral venous blood samples for DHEA, DHEA-S and cortisol determination were collected from first-time hospitalized adolescents with diagnoses of schizophrenia as well as from patients with conduct disorder. Patients were rated with the Positive and Negative Syndrome Scale (PANSS), ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495094</comments>
            <pubDate>Mon, 06 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495094</guid>        </item>
        <item>
            <title>DHEA and DHEA-S levels in hospitalized adolescents with first-episode schizophrenia and conduct disorder: A comparison study.</title>
            <link>http://www.medworm.com/index.php?rid=2316291&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19351578%26dopt%3DAbstract</link>
            <description>Authors: Strous RD, Maayan R, Kaminsky M, Blumensohn R, Weizman A, Spivak B
    
    PMID: 19351578 [PubMed - as supplied by publisher] (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316291</comments>
            <pubDate>Sun, 05 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316291</guid>        </item>
        <item>
            <title>Zolmitriptan compared to propranolol in the treatment of acute neuroleptic-induced akathisia: A comparative double-blind study</title>
            <link>http://www.medworm.com/index.php?rid=2495091&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000674%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuroleptic-induced akathisia (NIA) is a common, sometimes incapacitating adverse effect of anti-psychotic medication. Zolmitriptan is a selective 5-HT1D agonist. We aimed to determine its anti-NIA efficacy in comparison to propranolol. Thirty-three neuroleptic-treated patients were randomly allocated in a double-blind design to receive either 7.5 mg/d of zolmitriptan or 120 mg/d of propranolol for 3 consecutive days, followed by 3 days without any anti-NIA treatment. Patients were assessed at baseline and on days 3 and 7 by the Barnes Akathisia Rating Scale (BARS), PANSS, HAMD, HAMA, Pulse, and Blood Pressure. Both groups showed improvement of akathisia (BARS) along the treatment period, with significant effect for time but not for group. No significant differences were found...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495091</comments>
            <pubDate>Thu, 02 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495091</guid>        </item>
        <item>
            <title>Mirtazapine and paroxetine in major depression: A comparison of monotherapy versus their combination from treatment initiation</title>
            <link>http://www.medworm.com/index.php?rid=2495089&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000327%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: This double-blind study compared initial combination therapy against monotherapy using two antidepressant drugs with complementary mechanisms of action on the serotonin (5-HT) and norepinephrine (NE) systems. Sixty one adult patients with a DSM-IV diagnosis of unipolar depression were randomized to receive mirtazapine (30 mg/day), paroxetine (20 mg/day), or the combination of both drugs for 6 weeks. Response at week 4 was defined as a 30% reduction in the Montgomery-Asberg Depression Rating Scale (MADRS), and at week 6 as a 50% reduction in the MADRS. Remission was defined as a reduction in the MADRS score to 10 points or less. After 4 weeks, non-responders in the monotherapy groups had their medication dose increased by 50%. After 6 weeks, non-responders on monotherapy had ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2495089</comments>
            <pubDate>Thu, 02 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2495089</guid>        </item>
        <item>
            <title>Mirtazapine and paroxetine in major depression: A comparison of monotherapy versus their combination from treatment initiation.</title>
            <link>http://www.medworm.com/index.php?rid=2316293&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19345072%26dopt%3DAbstract</link>
            <description>Authors: Blier P, Gobbi G, Turcotte JE, de Montigny C, Boucher N, H&amp;#xE9;bert C, Debonnel G
    This double-blind study compared initial combination therapy against monotherapy using two antidepressant drugs with complementary mechanisms of action on the serotonin (5-HT) and norepinephrine (NE) systems. Sixty one adult patients with a DSM-IV diagnosis of unipolar depression were randomized to receive mirtazapine (30 mg/day), paroxetine (20 mg/day), or the combination of both drugs for 6 weeks. Response at week 4 was defined as a 30% reduction in the Montgomery-Asberg Depression Rating Scale (MADRS), and at week 6 as a 50% reduction in the MADRS. Remission was defined as a reduction in the MADRS score to 10 points or less. After 4 weeks, non-responders in the monotherapy groups had their me...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316293</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316293</guid>        </item>
        <item>
            <title>Zolmitriptan compared to propranolol in the treatment of acute neuroleptic-induced akathisia: A comparative double-blind study.</title>
            <link>http://www.medworm.com/index.php?rid=2316294&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342206%26dopt%3DAbstract</link>
            <description>Authors: Avital A, Gross-Isseroff R, Stryjer R, Hermesh H, Weizman A, Shiloh R
    Neuroleptic-induced akathisia (NIA) is a common, sometimes incapacitating adverse effect of anti-psychotic medication. Zolmitriptan is a selective 5-HT(1D) agonist. We aimed to determine its anti-NIA efficacy in comparison to propranolol. Thirty-three neuroleptic-treated patients were randomly allocated in a double-blind design to receive either 7.5 mg/d of zolmitriptan or 120 mg/d of propranolol for 3 consecutive days, followed by 3 days without any anti-NIA treatment. Patients were assessed at baseline and on days 3 and 7 by the Barnes Akathisia Rating Scale (BARS), PANSS, HAMD, HAMA, Pulse, and Blood Pressure. Both groups showed improvement of akathisia (BARS) along the treatment period, with significant ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316294</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Intranasal application of dopamine reduces activity and improves attention in Naples High Excitability rats that feature the mesocortical variant of ADHD</title>
            <link>http://www.medworm.com/index.php?rid=2746992&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000662%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, intranasal application of DA reduced hyperactivity at the highest dose used, whereas the intermediate dose improved attention in an animal model of ADHD. These results suggest the potential of employing intranasal DA for therapeutic purposes. (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2746992</comments>
            <pubDate>Mon, 30 Mar 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2746992</guid>        </item>
        <item>
            <title>Amelioration of cognitive deficits and neurodegeneration by curcumin in rat model of sporadic dementia of Alzheimer's type (SDAT)</title>
            <link>http://www.medworm.com/index.php?rid=2636734&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000492%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recent evidence indicates that curcumin (CUR), the principal curcuminoid of turmeric, exhibits antioxidant potential and protects the brain against various oxidative stressors. The aim of the present study was to examine the modulating impacts of CUR against cognitive deficits and oxidative damage in intracerebroventricular–streptozotocin (ICV–STZ) infused rats. Rats were injected bilaterally with ICV–STZ (3 mg/kg), while sham rats received the same volume of vehicle and then supplemented with CUR (80 mg/kg) for three weeks. After two weeks of ICV–STZ infusion, rats were tested for cognitive performance using passive avoidance and water maze tasks and then sacrificed for biochemical and histopathological assays. ICV–STZ rats showed significant cognitive deficits, whic...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2636734</comments>
            <pubDate>Mon, 30 Mar 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2636734</guid>        </item>
        <item>
            <title>Intranasal application of dopamine reduces activity and improves attention in Naples High Excitability rats that feature the mesocortical variant of ADHD.</title>
            <link>http://www.medworm.com/index.php?rid=2316298&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19328660%26dopt%3DAbstract</link>
            <description>In conclusion, intranasal application of DA reduced hyperactivity at the highest dose used, whereas the intermediate dose improved attention in an animal model of ADHD. These results suggest the potential of employing intranasal DA for therapeutic purposes.
    PMID: 19328660 [PubMed - as supplied by publisher] (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316298</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316298</guid>        </item>
        <item>
            <title>Amelioration of cognitive deficits and neurodegeneration by curcumin in rat model of sporadic dementia of Alzheimer's type (SDAT).</title>
            <link>http://www.medworm.com/index.php?rid=2316296&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329286%26dopt%3DAbstract</link>
            <description>Authors: Ishrat T, Hoda MN, Khan MB, Yousuf S, Ahmad M, Khan MM, Ahmad A, Islam F
    Recent evidence indicates that curcumin (CUR), the principal curcuminoid of turmeric, exhibits antioxidant potential and protects the brain against various oxidative stressors. The aim of the present study was to examine the modulating impacts of CUR against cognitive deficits and oxidative damage in intracerebroventricular-streptozotocin (ICV-STZ) infused rats. Rats were injected bilaterally with ICV-STZ (3 mg/kg), while sham rats received the same volume of vehicle and then supplemented with CUR (80 mg/kg) for three weeks. After two weeks of ICV-STZ infusion, rats were tested for cognitive performance using passive avoidance and water maze tasks and then sacrificed for biochemical and histopathological ...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316296</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316296</guid>        </item>
        <item>
            <title>The influence of psychiatric comorbidity on the dexamethasone/CRH test in major depression.</title>
            <link>http://www.medworm.com/index.php?rid=2316302&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19327969%26dopt%3DAbstract</link>
            <description>Authors: Veen G, Derijk RH, Giltay EJ, van Vliet IM, van Pelt J, Zitman FG
    
    PMID: 19327969 [PubMed - as supplied by publisher] (Source: European Neuropsychopharmacology)</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316302</comments>
            <pubDate>Wed, 25 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316302</guid>        </item>
        <item>
            <title>Research in anxiety disorders: From the bench to the bedside.</title>
            <link>http://www.medworm.com/index.php?rid=2316300&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19327970%26dopt%3DAbstract</link>
            <description>Authors: Garner M, M&amp;#xF6;hler H, Stein DJ, Mueggler T, Baldwin DS
    The development of ethologically based behavioural animal models has clarified the anxiolytic properties of a range of neurotransmitter and neuropeptide receptor agonists and antagonists, with several models predicting efficacy in human clinical samples. Neuro-cognitive models of human anxiety and findings from fMRI suggest dysfunction in amygdala-prefrontal circuitry underlies biases in emotion activation and regulation. Cognitive and neural mechanisms involved in emotion processing can be manipulated pharmacologically, and research continues to identify genetic polymorphisms and interactions with environmental risk factors that co-vary with anxiety-related behaviour and neuro-cognitive endophenotypes. This paper descr...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2316300</comments>
            <pubDate>Wed, 25 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2316300</guid>        </item>
        <item>
            <title>Blood, adipose tissue and brain levels of the cannabinoid ligands WIN-55,212 and SR-141716A after their intraperitoneal injection in mice: Compound-specific and area-specific distribution within the brain</title>
            <link>http://www.medworm.com/index.php?rid=2519941&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000480%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cannabinoid ligands have wide ranging neural and behavioral effects; therefore, they are of substantial therapeutic interest. The levels of cannabinoids are tightly controlled in brain infusion and in vitro methodologies, although the studied dose-ranges are extremely wide (e.g. 0.4–470 nmol in brain infusion studies). The brain levels reached after systemic administration are virtually unknown. To investigate this issue, we injected intraperitoneally 3H-labeled WIN-55,212 and SR141716A (0.3, 1 and 3 mg/kg) and estimated their accumulation in the blood, adipose tissue and brain. Accumulation was dose-dependent. The largest amounts were found in the adipose tissue, while the levels seen in the blood and brain were approximately similar. The accumulation of SR141716A was marked...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519941</comments>
            <pubDate>Mon, 23 Mar 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2519941</guid>        </item>
        <item>
            <title>Blood, adipose tissue and brain levels of the cannabinoid ligands WIN-55,212 and SR-141716A after their intraperitoneal injection in mice: Compound-specific and area-specific distribution within the brain.</title>
            <link>http://www.medworm.com/index.php?rid=2291269&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19303746%26dopt%3DAbstract</link>
            <description>Authors: Barna I, Till I, Haller J
    Cannabinoid ligands have wide ranging neural and behavioral effects; therefore, they are of substantial therapeutic interest. The levels of cannabinoids are tightly controlled in brain infusion and in vitro methodologies, although the studied dose-ranges are extremely wide (e.g. 0.4-470 nmol in brain infusion studies). The brain levels reached after systemic administration are virtually unknown. To investigate this issue, we injected intraperitoneally (3)H-labeled WIN-55,212 and SR141716A (0.3, 1 and 3 mg/kg) and estimated their accumulation in the blood, adipose tissue and brain. Accumulation was dose-dependent. The largest amounts were found in the adipose tissue, while the levels seen in the blood and brain were approximately similar. The accumulat...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2291269</comments>
            <pubDate>Thu, 19 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2291269</guid>        </item>
        <item>
            <title>Interactions between the glycine transporter 1(GlyT1) inhibitor SSR504734 and psychoactive drugs in mouse motor behaviour</title>
            <link>http://www.medworm.com/index.php?rid=2519945&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000649%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The specific glycine transporter 1 (GlyT1) inhibitor, SSR504734, is highly effective in enhancing N-methyl-d-aspartate receptor (NMDAR) function by elevating the availability of the NMDAR co-agonist, glycine, in the vicinity of NMDAR-containing glutamatergic synapses. According to the glutamatergic hypofunction hypothesis of schizophrenia, SSR504734 may therefore possess antipsychotic potential. Here, we evaluated the effects of SSR504734 in response to three psychomimetic drugs: phencyclidine, amphetamine, and apomorphine in male C57BL/6 mice. SSR504734 attenuated phencyclidine-induced (5 mg/kg, i.p.) hyperlocomotion, but potentiated the motor stimulant and motor depressant effects of amphetamine (2.5 mg/kg, i.p.) and apomorphine (0.75 mg/kg, s.c.), respectively. Hence, SSR50...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519945</comments>
            <pubDate>Thu, 12 Mar 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Hippocampal nAChRs mediate nicotine withdrawal-related learning deficits</title>
            <link>http://www.medworm.com/index.php?rid=2519943&amp;cid=s_35556_36_f&amp;fid=35556&amp;url=http%3A%2F%2Fwww.europeanneuropsychopharmacology.com%2Farticle%2FPIIS0924977X09000637%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Nicotine modulation of learning may contribute to its abuse liability. The role of hippocampal nicotinic acetylcholine receptors (nAChRs) in the effects of acute, chronic and withdrawal from chronic nicotine on learning was assessed via intrahippocampal drug infusion in mice. Acute dorsal hippocampal nicotine infusion enhanced contextual fear conditioning. Conversely, chronic intrahippocampal infusion of a matched dose had no effect, and withdrawal from chronic infusion impaired learning. Thus, hippocampal functional adaptation, evidenced by learning deficits during abstinence, occurs with the transition from acute to chronic nicotine exposure. To investigate which hippocampal nAChRs mediate these adaptations, C57BL/6, β2 nAChR subunit knockout (KO), and wildtype (WT) mice treat...</description>
            <author>European Neuropsychopharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2519943</comments>
            <pubDate>Thu, 12 Mar 2009 00:00:00 +0100</pubDate>
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