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        <title>Neuropeptides 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 'Neuropeptides' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Neuropeptides&t=Neuropeptides&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 16:33:19 +0100</lastBuildDate>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=3311447&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417910000144%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311447</comments>
            <pubDate>Fri, 26 Feb 2010 16:56:48 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3311425&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417910000119%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311425</comments>
            <pubDate>Fri, 26 Feb 2010 16:56:45 +0100</pubDate>
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        <item>
            <title>Compensatory mechanisms to maintain blood pressure in paraplegic rats: Implication of central tachykinin NK-1 and NK-3 receptors?</title>
            <link>http://www.medworm.com/index.php?rid=3311445&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001516%2Fabstract%3Frss%3Dyes</link>
            <description>This study examined the intracerebroventricular (i.c.v.) effects of the selective NK-1 receptor agonist [Sar9, Met(O2)11]SP (65pmol, n=6) and NK-3 receptor agonist senktide (650pmol, n=6) on mean arterial pressure (MAP) and HR before and after complete spinal cord transection at thoracic level 4 (T4). [Sar9, Met(O2)11]SP evoked increases in MAP and HR which were still present 4days after the T4 SCI. Further analysis using the β1-adrenoceptor antagonist atenolol (10mgkg−1) revealed an increased contribution of HR in the MAP increase after SCI. For senktide, 2 and 5weeks after T4 SCI, the rise in MAP induced by senktide was significantly increased in magnitude and was similar to a normal response at 8weeks. These effects were accompanied by a bradycardia, which was still present and ampli...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311445</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311445</guid>        </item>
        <item>
            <title>Antidiabetic efficacy of bradykinin antagonist R-954 on glucose tolerance test in diabetic type 1 mice</title>
            <link>http://www.medworm.com/index.php?rid=3311443&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001498%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Insulin-dependent diabetes mellitus (type 1 diabetes) is an inflammatory autoimmune disease associated with many complications including nephropathy, retinopathy, neuropathy and hyperalgesia. Experimental evidence has shown that the bradykinin B1 receptor (BKB1-R) is involved in the development of type 1 diabetes and found to be upregulated alongside the disease. In the present study the effects of the selective BKB1-R antagonist the R-954 (Ac-Orn-[Oic2, α-MePhe5, D-β Nal7, Ile8 ]des-Arg9-BK and the BKB1-R agonist des Arg9-BK (DBK) were studied on diabetic hyperglycemia. Diabetic type 1 was induced in C57 BL/KsJ mdb male mice by five consecutives doses of STZ (45mg/kg i.p.). A glucose tolerance test (GTT) was performed by an intraperitoneal administration of glucose, 8, 12 and ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311443</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311443</guid>        </item>
        <item>
            <title>Selective tumor blood–brain barrier opening with the kinin B2 receptor agonist [Phe8ψ(CH2NH)Arg9]-BK in a F98 glioma rat model: An MRI study</title>
            <link>http://www.medworm.com/index.php?rid=3311442&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001486%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Treatment of malignant glioma with chemotherapy is limited mostly because of delivery impediment related to the blood–brain barrier (BBB). One approach for transporting drugs across the BBB involves the activation of bradykinin-B2 receptors (BK-B2R). Our objective was to pharmacologically characterize the BBB permeability induced by the synthetic biostable BK-B2R analogue [Phe8ψ(CH2NH)Arg9]-BK (R523) in F98 glioma-implanted Fischer rats. On day 10 post-inoculation, we detected the presence of B2R in the tumor cells and the peritumoral microvasculature (RT-PCR and immunohistochemistry). We assessed BBB permeability before and after the intracarotid (i.c.) infusion of R523 (0.1ml/min for 5min; 2.5, 10, and 50nmol/kg/min) using non-invasive dynamic contrast-enhanced magnetic reso...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311442</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311442</guid>        </item>
        <item>
            <title>Contribution of the central dopaminergic system in the anti-hypertensive effect of kinin B1 receptor antagonists in two rat models of hypertension</title>
            <link>http://www.medworm.com/index.php?rid=3311444&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001504%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Kinins are neuroactive peptides that could play a role in central autonomic control of blood pressure. Whereas kinin B1R binding sites were increased in specific brain areas of spontaneously hypertensive rats (SHR) and Angiotensin II (AngII)-hypertensive rats, the contribution of kinin B1R in hypertension remains controversial. The aims of the study were to determine: (a) the effects on mean arterial blood pressure (MAP) of centrally and peripherally administered B1R antagonists in SHR (16weeks) and AngII-hypertensive rats (200ng/kg/min×2weeks, s.c.); (b) the contribution of central dopamine in the effects of SSR240612. The rationale is based on the overactivity of the dopaminergic system in hypertension. In both models, SSR240612 (1, 5 and 10mg/kg, gavage) reduced dose-dependen...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311444</comments>
            <pubDate>Thu, 14 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311444</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=3166836&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001607%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166836</comments>
            <pubDate>Wed, 13 Jan 2010 16:37:05 +0100</pubDate>
            <guid isPermaLink="false">3166836</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3166826&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001577%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166826</comments>
            <pubDate>Wed, 13 Jan 2010 16:37:04 +0100</pubDate>
            <guid isPermaLink="false">3166826</guid>        </item>
        <item>
            <title>Akt pathway activation and increased neuropeptide Y mRNA expression in the rat hippocampus: Implications for seizure blockade</title>
            <link>http://www.medworm.com/index.php?rid=3311441&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001462%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The aim of this study was to analyze the expression of survival-related molecules such Akt and integrin-linked kinase (ILK) to evaluate Akt pathway activation in epileptogenesis process. Furthermore, was also investigated the mRNA expression of neuropeptide Y, a considered antiepileptic neuropeptide, in the pilocarpine-induced epilepsy. Male Wistar rats were submitted to the pilocarpine model of epilepsy. Hippocampi were removed 6h (acute phase), 12h (late acute), 5d (silent) and 60d (chronic) after status epilepticus (SE) onset, and from animals that received pilocarpine but did not develop SE (partial group). Hippocampi collected were used to specify mRNA expression using Real-Time PCR. Immunohistochemistry assay was employed to place ILK distribution in the hippocampus and Wes...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311441</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311441</guid>        </item>
        <item>
            <title>Role of kinin B1 and B2 receptors in memory consolidation during the aging process of mice</title>
            <link>http://www.medworm.com/index.php?rid=3311440&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001450%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Under physiological conditions, elderly people present memory deficit associated with neuronal loss. This pattern is also associated with Alzheimer’s disease but, in this case, in a dramatically intensified level. Kinin receptors have been involved in neurodegeneration and increase of amyloid-β concentration, associated with Alzheimer’s disease (AD). Considering these findings, this work evaluated the role of kinin receptors in memory consolidation during the aging process. Male C57Bl/6 (wt), knock-out B1 (koB1) or B2 (koB2) mice (3, 6, 12 and 18-month-old – mo; n=10 per group) were submitted to an acquisition session, reinforcement to learning (24h later: test 1) and final test (7days later: test 2), in an active avoidance apparatus, to evaluate memory. Conditioned avoida...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311440</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311440</guid>        </item>
        <item>
            <title>Plasma Kallikrein and Angiotensin I-converting enzyme N- and C-terminal domain activities are modulated by the insertion/deletion polymorphism</title>
            <link>http://www.medworm.com/index.php?rid=3311437&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001425%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Angiotensin I-converting enzyme (ACE) is recognized as one of the main effector molecules involved in blood pressure regulation. In the last few years some polymorphisms of ACE such as the insertion/deletion (I/D) polymorphism have been described, but their physiologic relevance is poorly understood. In addition, few studies investigated if the specific activity of ACE domain is related to the I/D polymorphism and if it can affect other systems. The aim of this study was to establish a biochemical and functional characterization of the I/D polymorphism and correlate this with the corresponding ACE activity. For this purpose, 119 male brazilian army recruits were genotyped and their ACE plasma activities evaluated from the C- and N-terminal catalytic domains using fluorescence res...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311437</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311437</guid>        </item>
        <item>
            <title>Effect of kinin B2 receptor ablation on skeletal muscle development and myostatin gene expression</title>
            <link>http://www.medworm.com/index.php?rid=3311446&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001401%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, together our results show that kinin B2 receptor deletion increases lean mass, reduces fat mass and improves metabolism efficiency in mice. The mechanism involved in this phenotype could be related to the reduction of myostatin gene expression during postnatal life. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311446</comments>
            <pubDate>Mon, 04 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311446</guid>        </item>
        <item>
            <title>Distribution and expression of B2-kinin receptor on human leukocyte subsets in young adults and elderly using flow cytometry</title>
            <link>http://www.medworm.com/index.php?rid=3311439&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001449%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The kallikrein-kinin system has been investigated in many experimental models. Dysregulations of the KKS are likely to be involved in pathologies such as inflammation, cancer and cardiovascular diseases. Previous works on the human KKS mostly rely on gene polymorphism and mRNA expression. In order to assess the KKS in human at the protein level, we have developed an approach based on flow cytometric analysis of leukocytes. Whole blood samples were collected and erythrocytes were lysed. Permeabilised leukocytes were incubated with anti-B2R (IgG2b), anti-IgG2b-PE, anti-CD3-PerCP (lymphocytes) and anti-CD14-APC (monocytes) antibodies. FACScalibur analyzed fluorescence intensities. Results were expressed as per cent of B2R-positive cells in each leukocyte subset and as B2R fluorescen...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311439</comments>
            <pubDate>Mon, 04 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311439</guid>        </item>
        <item>
            <title>Differential regulation of inducible and endothelial nitric oxide synthase by kinin B1 and B2 receptors</title>
            <link>http://www.medworm.com/index.php?rid=3311438&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001437%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Kinins are vasoactive peptides that play important roles in cardiovascular homeostasis, pain and inflammation. After release from their precursor kininogens, kinins or their C-terminal des-Arg metabolites activate two distinct G protein-coupled receptors (GPCR), called B2 (B2R) or B1 (B1R). The B2R is expressed constitutively with a wide tissue distribution. In contrast, the B1R is not expressed under normal conditions but is upregulated by tissue insult or inflammatory mediators. The B2R is considered to mediate many of the acute effects of kinins while the B1R is more responsible for chronic responses in inflammation. Both receptors can couple to Gαi and Gαq families of G proteins to release mediators such as nitric oxide (NO), arachidonic acid, prostaglandins, leukotrienes a...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311438</comments>
            <pubDate>Mon, 04 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311438</guid>        </item>
        <item>
            <title>Neuronal circuits involving ghrelin in the hypothalamus-mediated regulation of feeding</title>
            <link>http://www.medworm.com/index.php?rid=3311436&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001395%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Ghrelin, an n-octanoylated 28-amino acid brain–gut peptide, was first isolated from extracts of porcine stomach. Ghrelin is an endogenous ligand for the growth hormone secretagogue type 1a receptor (GHS-R1a), the functionally active form of GHS-R, and stimulates feeding and growth hormone secretion. Ghrelin is mainly produced in the A/X-like cells of the oxyntic glands of the stomach and is the main orexigenic circulating hormone that acts on the hypothalamus to affect feeding behavior and energy metabolism.Ghrelin-containing neuronal cell bodies are localized in the hypothalamic arcuate nucleus, a center that integrates signals for energy homeostasis. Ghrelin-containing nerve fibers are widely distributed in the brain. Accumulated evidence shows that hypothalamic neuropeptides...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311436</comments>
            <pubDate>Fri, 25 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311436</guid>        </item>
        <item>
            <title>VPAC1 receptor binding site: Contribution of photoaffinity labeling approach</title>
            <link>http://www.medworm.com/index.php?rid=3311435&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001371%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The vasoactive intestinal peptide (VIP) is a prominent 28 aminoacid neuropeptide with wide distribution in both central and peripheral nervous systems, where it plays important regulatory role in many physiological processes. VIP has a large spectrum of biological functions including exocrine secretions, hormone release, foetal development, immune response and also exerts beneficial effect in neuro-degenerative and inflammatory diseases. Few years ago, it has been shown that VIP can be a promising anti-inflammatory agent. VIP mechanisms of action implicate two sub-types of receptors (VPAC1 and VPAC2) which are members of class B receptors belonging to the super-family of G protein-coupled receptor (GPCR). Because, VPAC1 receptor plays an important role in the modulation of the an...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311435</comments>
            <pubDate>Fri, 25 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311435</guid>        </item>
        <item>
            <title>Kinins in cardiac inflammation and regeneration: Insights from ischemic and diabetic cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=3311434&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS014341790900136X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The kallikrein–kinin system (KKS) is a system of vasoactive peptides, the kinins, involved in different aspects of remodeling, inflammation and angiogenesis. Kinins mediate their actions through two receptors, B1R and B2R. It is increasingly recognized that the KKS is involved in the inflammatory processes of the heart. Evidence shows that the B2R is beneficial in myocardial diseases, protecting from inflammation, fibrosis and apoptosis, while B1R shows a proinflammatory character contributing to the disease progression by increasing the production of cytokines and stimulating the migration of immune cells. Furthermore, novel important actions of the KKS and its receptors contribute to neovascularization and recruitment of endothelial progenitor cells in ischemic areas and endo...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311434</comments>
            <pubDate>Fri, 25 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311434</guid>        </item>
        <item>
            <title>Ethanol exposure selectively alters β-endorphin content but not [3H]-DAMGO binding in discrete regions of the rat brain</title>
            <link>http://www.medworm.com/index.php?rid=3166828&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001383%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The dopaminergic mesocorticolimbic system plays an important role in the reinforcing effects of ethanol. Opioid peptides modulate the activity of this system and have been suggested to mediate, at least in part, the reinforcing properties of ethanol. Thus, beta-endorphin (β-END) could participate in the development of ethanol reinforcement and addiction. The aim of this work was to investigate the acute and chronic ethanol effects on β-END content in regions of the mesolimbic system and to examine if chronic ethanol treatment alters ligand binding to mu opioid receptor (μOR). Male Wistar rats received a single acute ethanol dose of 2.5g/kg or water by intra-gastric administration. For chronic ethanol treatment experiments, one group of rats was given ethanol (10% v/v solution)...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166828</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166828</guid>        </item>
        <item>
            <title>Structural analysis of three peptides related to the transmambranic helix VI of AT1 receptor</title>
            <link>http://www.medworm.com/index.php?rid=3311433&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001358%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Strong correlation was found in the results of biochemical, cellular and structural approaches used to compare WT AT1R to mutant types. Random coil structure of the L265D mutant may be a key point to explain those changes observed in biochemical (binding and signal transduction) and proliferation assays (). β-Turn formation is an important step during early protein folding and this secondary simple structure is present in L262D and WT, but not in L265D. Therefore, leucine 265 seems to play a crucial role in determining an entirely functional AT1R. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311433</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311433</guid>        </item>
        <item>
            <title>Corrigendum to “Role of NGF in spared DRG following partial dorsal rhizotomy in cats” [Neuropeptides 43(5) (2009) 363–369]</title>
            <link>http://www.medworm.com/index.php?rid=3166835&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001322%2Fabstract%3Frss%3Dyes</link>
            <description>The affiliation for the first author (Xue Zhou) is hereby replaced with the following:  Department of Histology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166835</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166835</guid>        </item>
        <item>
            <title>Genome-wide census and expression profiling of chicken neuropeptide and prohormone convertase genes</title>
            <link>http://www.medworm.com/index.php?rid=3166831&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001310%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuropeptides regulate cell-cell signaling and influence many biological processes in vertebrates, including development, growth, and reproduction. The complex processing of neuropeptides from prohormone proteins by prohormone convertases, combined with the evolutionary distance between the chicken and mammalian species that have experienced extensive neuropeptide research, has led to the empirical confirmation of only 18 chicken prohormone proteins. To expand our knowledge of the neuropeptide and prohormone convertase gene complement, we performed an exhaustive survey of the chicken genomic, EST, and proteomic databases using a list of 95 neuropeptide and 7 prohormone convertase genes known in other species. Analysis of the EST resources and 22 microarray studies offered a compr...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166831</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166831</guid>        </item>
        <item>
            <title>Differential effect of prolonged food restriction and fasting on hypothalamic malonyl-CoA concentration and expression of orexigenic and anorexigenic neuropeptides genes in rats</title>
            <link>http://www.medworm.com/index.php?rid=3166829&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001346%2Fabstract%3Frss%3Dyes</link>
            <description>This study examined the effect of prolonged food restriction, common in humans trying to lose body weight on expression of orexigenic and anorexigenic neuropetides genes and on malonyl-CoA content in rat whole hypothalamus.We observed an increase of NPY and AgRP mRNA levels in hypothalamus of rats kept on 30days-long food restriction (50% of the amount of food consumed by controls). Simultaneously, a decrease of CART and POMC mRNA levels occurred. Refeeding caused a decrease in NPY and POMC mRNA levels without effect on AgRP and CART mRNA. Surprisingly, both prolonged food restriction and food restriction/refeeding caused the increase of malonyl-CoA level in whole hypothalamus. In contrast, fasting for 24h caused the decrease of malonyl-CoA level, which was associated with the up-regulatio...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166829</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166829</guid>        </item>
        <item>
            <title>Endomorphin-suppressed nitric oxide release from mice peritoneal macrophages</title>
            <link>http://www.medworm.com/index.php?rid=3166830&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001334%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Endomorphins are newly discovered μ-opioid receptor selective immunocompetent opioid peptides. Endomorphin 1 is predominantly distributed in brain, while endomorphin 2 is widely allocated in the spinal cord. Lately, endomorphins have been investigated as modulators of reactive oxygen and nitrogen species. Nitric oxide is short lived radical involved in various biological processes such as regulation of blood vessel contraction, inflammation, neurotransmission and apoptosis. The aim of this work was to investigate the in vivo effects of endomorphins on nitric oxide release and NOS 2 isoenzyme upregulation in mice peritoneal macrophages additionally challenged ex vivo with lipopolysaccharide. The results showed that endomorphin 1 or endomorphin 2 in vitro did not change NO release...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166830</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166830</guid>        </item>
        <item>
            <title>Bradykinin B1 receptor antagonist R954 inhibits eosinophil activation/proliferation/migration and increases TGF-β and VEGF in a murine model of asthma</title>
            <link>http://www.medworm.com/index.php?rid=3311432&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001309%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In the present study the effects of bradykinin receptor antagonists were investigated in a murine model of asthma using BALB/c mice immunized with ovalbumin/alum and challenged twice with aerosolized ovalbumin. Twenty four hours later eosinophil proliferation in the bone marrow, activation (lipid bodies formation), migration to lung parenchyma and airways and the contents of the pro-angiogenic and pro-fibrotic cytokines TGF-β and VEGF were determined. The antagonists of the constitutive B2 (HOE 140) and inducible B1 (R954) receptors were administered intraperitoneally 30min before each challenge. In sensitized mice, the antigen challenge induced eosinophil proliferation in the bone marrow, their migration into the lungs and increased the number of lipid bodies in these cells. Th...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311432</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311432</guid>        </item>
        <item>
            <title>Distribution of neuropeptide W in the rat brain</title>
            <link>http://www.medworm.com/index.php?rid=3311431&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001164%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we used RT-PCR analysis to examine the gene expression of NPW mRNA in the rat brain, and performed a detailed analysis of the distribution of NPW-positive neurons by use of immunohistochemistry at both the light and electron microscopic levels. NPW mRNA expression was demonstrated in the hypothalamic paraventricular nucleus (PVN), arcuate nucleus (ARC), ventromedial nucleus (VMH) and lateral hypothalamus (LH). At the light microscopic level, NPW-like immunoreactive (NPW-LI) cell bodies were found in the preoptic area (POA), PVN, ARC, VMH, LH, PMD (dorsal premammillary nucleus), periaqueductal gray (PAG), lateral parabrachial nucleus (LPB), and prepositus nucleus (Pr). NPW-LI axon terminals were shown in the POA, bed nucleus of the stria terminalis (BST), amygdala, PVN, ARC, ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311431</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311431</guid>        </item>
        <item>
            <title>Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-β 1-40 peptide in mice</title>
            <link>http://www.medworm.com/index.php?rid=3311430&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001152%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Chronic infusion of human amyloid-β 1-40 (Aβ) in the lateral ventricle (LV) of rats is associated with memory impairment and increase of kinin receptors in cortical and hippocampal areas. Deletion of kinin B1 or B2 receptors abolished memory impairment caused by an acute single injection of Aβ in the LV. As brain tissue and kinin receptors could unlikely react to acute or chronic administration of a similar quantity of Aβ, we evaluated the participation of B1 or B2 receptors in memory impairment after chronic infusion of Aβ. Male C57Bl/6J (wt), knock-out B1 (koB1) or B2 (koB2) mice (12weeks of age) previously trained in a two-way shuttle-box and achieving conditioned avoidance responses (CAR, % of 50 trials) were infused with AB (550pmol, 0.12μL/h, 28days) or vehicle in the...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311430</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311430</guid>        </item>
        <item>
            <title>Differential effects of substance P or hemokinin-1 on transient receptor potential channels, TRPV1, TRPA1 and TRPM8, in the rat</title>
            <link>http://www.medworm.com/index.php?rid=3166834&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001115%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Two tachykinin peptides, substance P (SP) and hemokinin-1 (HK-1), and three transient receptor potential (TRP) channels, TRPV1, TRPA1 and TRPM8, are similarly localized in the spinal dorsal horn and dorsal root ganglion, suggesting that TRP channels may be related or modulated by these tachykinin peptides. Thus, to clarify whether the responses of TRP channels are modulated by SP or HK-1, the effects of pretreatment with SP or HK-1 on the induction of scratching behavior by TRP channel agonists were examined. Pretreatment with SP or HK-1 enhanced the induction of scratching behavior by resiniferatoxin, a TRPV1 agonist, whereas scratching behavior induced by menthol, a TRPM8 agonist, was suppressed by pretreatment with these peptides. On the other hand, pretreatment with SP, but n...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166834</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166834</guid>        </item>
        <item>
            <title>PACAP and VIP affect NF1 expression in rat malignant peripheral nerve sheath tumor (MPNST) cells</title>
            <link>http://www.medworm.com/index.php?rid=3166832&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001127%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In our previous study we have identified PACAP, VIP and their receptors in rat malignant peripheral nerve sheath tumor (MPNST) cells, thus showing anti-apoptotic roles. Recently it has been shown that the tumor suppressor neurofibromin, encoded by the Neurofibromatosis type I (NF1) gene, promotes MPNST cells sensitivity to apoptosis after serum withdrawal.In the present study we investigated whether PACAP or VIP negatively regulate NF1 expression under normal or serum-dependent pro-apoptotic culture conditions. Results indicated that serum itself significantly influenced gene and protein levels. In fact, the low NF1 levels of cells cultured in normal serum-containing medium were remarkably increased in cells switched to low- or no-serum after 24h and 48h. Treatment with 100nM PAC...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166832</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166832</guid>        </item>
        <item>
            <title>Kinin B1 and B2 receptors contribute to orofacial heat hyperalgesia induced by infraorbital nerve constriction injury in mice and rats</title>
            <link>http://www.medworm.com/index.php?rid=3311429&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001140%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Mechanisms coupled to kinin B1 and B2 receptors have been implicated in sensory changes associated to various models of neuropathy. The current study aimed to investigate if kinins also participate in orofacial thermal hyperalgesia induced by constriction of the infraorbital nerve (CION), a model of trigeminal neuropathic pain which displays persistent hypersensitivity to orofacial sensory stimulation, in rats and mice. Male Swiss mice (30–35g) or Wistar rats (200–250g; n=6–10 per group in both cases) underwent CION or sham surgery and were submitted repeatedly to application of heat (∼50°C) to the ipsilateral or contralateral snout, delivered by a heat source placed 1cm from the vibrissal pad. Decreases in latency to display head withdrawal or vigorous snout flicking we...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311429</comments>
            <pubDate>Mon, 16 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311429</guid>        </item>
        <item>
            <title>Effect of serotonergic system on AVP secretion induced by physical exercise</title>
            <link>http://www.medworm.com/index.php?rid=3166833&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001139%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The present study was undertaken in order to establish the possible involvement of serotonergic receptors in the control of physical exercise-stimulated vasopressin secretion. Twenty-one healthy men (divided in three groups of seven) underwent bicycle-ergometer tests until exhaustion: exercise control test (n=21), exercise plus ondansetron, selective 5-HT3 antagonist (n=7), exercise plus buspirone, selective 5-HT1A receptor agonist (n=7), exercise plus sumatriptan, selective 5-HT1D receptor agonist (n=7). AVP levels, physiological and biochemical variables were measured and compared during tests. Results showed that exercise-induced AVP rise did not change after the administration of buspirone and sumatriptan. In contrast, the administration of ondansetron significantly reduced p...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166833</comments>
            <pubDate>Mon, 16 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166833</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=2973797&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001231%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973797</comments>
            <pubDate>Mon, 09 Nov 2009 16:47:58 +0100</pubDate>
            <guid isPermaLink="false">2973797</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2973790&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS014341790900119X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973790</comments>
            <pubDate>Mon, 09 Nov 2009 16:47:57 +0100</pubDate>
            <guid isPermaLink="false">2973790</guid>        </item>
        <item>
            <title>Neuropeptide Y receptor subtypes in the dorsal vagal complex under acute feeding adaptation in the adult rat</title>
            <link>http://www.medworm.com/index.php?rid=3311428&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001103%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuropeptide Y (NPY), Peptide YY (PYY) and pancreatic polypeptides (PPs) belong to the same peptide family called the Y or NPY family. Central and peripheral injections of these peptides are implicated in the regulation of food intake at the level of the hypothalamus (central effects; increased food intake) and dorsal vagal complex (DVC) (peripheral effects; decreased food intake). The DVC of the brainstem is a satiety reflex key region, which includes the nucleus tractus solitarius (NTS), area postrema (AP) and dorso motor nucleus of the vagus (DMX). NPY binding sites were quantified on serial DVC sections using in vitro receptor autoradiography in two feeding adaptation models: fasting and inflammatory anorexia. Receptor autoradiography revealed that Y1, Y2, Y4 and Y5 receptor ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311428</comments>
            <pubDate>Mon, 02 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311428</guid>        </item>
        <item>
            <title>The regulatory role of neurotensin on the hypothalamic–anterior pituitary axons: Emphasis on the control of thyroid-related functions</title>
            <link>http://www.medworm.com/index.php?rid=3166827&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001097%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neurotensin (NT) is a 13 amino acid neurohormone and/or neuromodulator, located in the synaptic vesicles and released from the neuronal terminals in a calcium-dependent manner. This peptide is present among mammalian and nonmammalian species, mainly in the central nervous system and the gastrointestinal tract. Due to its neuroendocrine activity, NT has been related to the pathophysiology of a series of disorders, such as schizophrenia, drug-abuse, Parkinson’s disease, cancer, stroke, eating disorders and other neurodegenerative conditions. Moreover, NT participates in the physiology of pain-induction, central blood pressure control and inflammation. NT also plays an important interactive role in all components of the hypothalamic–anterior pituitary circuit, which is mediated ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3166827</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3166827</guid>        </item>
        <item>
            <title>Glyceroltrinitrate facilitates stimulated CGRP release but not gene expression of CGRP or its receptor components in rat trigeminal ganglia</title>
            <link>http://www.medworm.com/index.php?rid=2973793&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001061%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Nitric oxide (NO) donors induce delayed headaches in migraineurs. In a corresponding rat model NO donors cause delayed ongoing activity in central trigeminal neurons which process intracranial afferent input. Cellular models indicate that NO may increase the release or production of calcitonin gene-related peptide (CGRP), a key mediator in primary headaches. CGRP release from intact isolated trigeminal ganglia of adult male Wistar rats was investigated in vitro. Exposure to high NO donor concentrations did not affect basal or stimulated CGRP release. After a two hour infusion of the NO donor glyceroltrinitrate (250μg/kg/h), however, inflammatory mediators-induced CGRP release was 80% higher compared to control animals. Administration of the soluble guanylate cyclase inhibitor OD...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973793</comments>
            <pubDate>Wed, 28 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973793</guid>        </item>
        <item>
            <title>Cloning and distribution of neuropeptide S and its receptor in the pig</title>
            <link>http://www.medworm.com/index.php?rid=2973792&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001073%2Fabstract%3Frss%3Dyes</link>
            <description>In this report, the cDNAs of NPS and NPSR were cloned and sequenced. Homology and phylogenetic analysis of NPS gene sequences were performed. The expression of NPS and NPSR mRNA in the pig was systemically investigated using semiquantitative reverse transcription polymerase chain reaction (RT-PCR), while the distribution of NPS was determined by immunohistochemistry. Our results demonstrated that the gene and predicted amino acid sequences of both NPS and NPSR were highly conserved. Phylogenetic analysis showed that NPS coding sequences from related species display high degrees of homology. NPS and NPSR mRNAs were widely expressed in various tissues of the pig. NPS mRNA was highly expressed in CNS, while NPSR mRNA was widely expressed in many tissues, with high expression in the hypophysis...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973792</comments>
            <pubDate>Mon, 26 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973792</guid>        </item>
        <item>
            <title>Guest Editorial for the Special Issue Peptide Receptors: Focus on Neuropeptides and Kinins</title>
            <link>http://www.medworm.com/index.php?rid=3311426&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000912%2Fabstract%3Frss%3Dyes</link>
            <description>The Joint International Symposium Peptide Receptors – Kinin 2009 was successfully held in Quebec City (June 26–30, 2009), and the Editor-in-Chief of Neuropeptides, Dr. Jacqueline N. Crawley, graciously accepted to host a Special Issue open to the 150 participants of this event. This was the 5th Symposium of the Peptide Receptors series and the preceding editions (1994, 1996, 2001, 2004) were all held in Montreal, Canada. The 2009 symposium benefited from the experience of a pretty stable core of members of the successive local organizing committees. The 2009 edition of Peptide Receptors was recognized as the First meeting of the Canadian Branch of the International Neuropeptide Society (www.inps.org). Thus, the usual interest in the neurosciences was strongly represented with cutting e...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311426</comments>
            <pubDate>Wed, 21 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311426</guid>        </item>
        <item>
            <title>Altered cardiac bradykinin metabolism in experimental diabetes caused by the variations of angiotensin-converting enzyme and other peptidases</title>
            <link>http://www.medworm.com/index.php?rid=3311427&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909001085%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The peptidases angiotensin-converting enzyme (ACE) and neutral endopeptidase 24.11 (NEP) mediate most of the kinin catabolism in normal cardiac tissue and are the molecular targets of inhibitory drugs that favorably influence diabetic complications. We studied the variations of those kininases in the myocardium of rats in experimental diabetes. ACE and NEP activities were significantly decreased in heart membranes 4–8weeks post-streptozotocin (STZ) injection. However, insulin-dependent diabetes did not modify significantly bradykinin (BK) half-life (t1/2) while the effect of both ACE (enalaprilat) and ACE and NEP (omapatrilat) inhibitors on BK degradation progressively decreased, which may be explained by the upregulation of other unidentified metallopeptidase(s). In vivo insul...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3311427</comments>
            <pubDate>Mon, 19 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3311427</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=2915957&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000973%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915957</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915957</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2915949&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000948%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915949</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915949</guid>        </item>
        <item>
            <title>Evidence from knockout mice for distinct implications of neuropeptide-Y Y2 and Y4 receptors in the circadian control of locomotion, exploration, water and food intake</title>
            <link>http://www.medworm.com/index.php?rid=2973794&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000900%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Members of the neuropeptide-Y (NPY) family acting via Y2 and/or Y4 receptors have been proposed to participate in the control of ingestive behaviour and energy homeostasis. Since these processes vary between day and night, we explored the circadian patterns of locomotor, exploratory and ingestive behaviour in mice with disrupted genes for Y2 (Y2−/−) or Y4 (Y4−/−) receptors. To this end, the LabMaster system was used and its utility for the analysis of changes in circadian activity and ingestion caused by gene knockout evaluated. Female animals, aged 27weeks on average, were housed singly in cages fitted with sensors for water and food intake and two infrared frames for recording ambulation and rearing under a 12h light/dark cycle for 4days. Relative to WT animals, diurnal...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973794</comments>
            <pubDate>Fri, 25 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973794</guid>        </item>
        <item>
            <title>NPY regulation of bone remodelling</title>
            <link>http://www.medworm.com/index.php?rid=2973791&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000894%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuropeptide Y (NPY), a classic neuronal regulator of energy homeostasis, is now also known to be involved in the control of bone homeostasis. Of the five known Y receptors through which the NPY family of ligands signals, the Y1 and Y2 receptors have so far been implicated in the control of osteoblast activity and thus bone formation. Analysis of brain specific NPY overexpressing and Y receptor knockout models has revealed a powerful anabolic pathway likely involving hypothalamic Y2 receptors and osteoblastic Y1 receptors. Furthering our understanding of the mechanisms underlying the involvement of the NPY system in the control of bone could lead to the development of therapies to improve bone mass in patients with diseases such as osteoporosis. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973791</comments>
            <pubDate>Mon, 14 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973791</guid>        </item>
        <item>
            <title>Stimulatory effect of growth hormone–releasing hormone (GHRH(1-29)NH2) on the proliferation, VEGF and chromogranin A secretion by human neuroendocrine tumor cell line NCI-H727 in vitro</title>
            <link>http://www.medworm.com/index.php?rid=2915955&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000882%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Growth hormone–releasing hormone (GHRH) and its receptors have been implicated in a variety of cellular processes like cell survival, proliferation, apoptosis, angiogenesis and neoplastic transformation of various non-pituitary tissues. Here, we investigated for the first time the in vitro effect of GHRH(1-29)NH2 on the proliferation and the secretion of vascular endothelial growth factor (VEGF) and chromogranin A by the human bronchial neuroendocrine tumor cells NCI-H727. GHRH(1-29)NH2 at the concentrations of 10−8–10−6M increased the proliferation of these cells and this effect was associated with a statistically significant increase in VEGF and chromogranin A secretion into the supernatants of the tested cells. Our findings indicate that GHRH functions as a trophic hor...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915955</comments>
            <pubDate>Thu, 10 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915955</guid>        </item>
        <item>
            <title>Poster abstracts</title>
            <link>http://www.medworm.com/index.php?rid=2915956&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000869%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915956</comments>
            <pubDate>Wed, 09 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915956</guid>        </item>
        <item>
            <title>Nociceptin/orphanin FQ and NOP receptor gene regulation after acute or repeated social defeat stress</title>
            <link>http://www.medworm.com/index.php?rid=2973796&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000845%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antagonists of the NOP receptor have antidepressant effects in rodent models, suggesting that the N/OFQ–NOP system may play an important role in affective disorders. Furthermore, multiple lines of experimental evidence link N/OFQ neurotransmission with physiological and behavioral responses to stress. One possibility is that disregulated expression of the N/OFQ peptide neurotransmitter and/or the NOP receptor may participate in the etiology of stress-induced psychopathology. In the present set of experiments, we compared gene expression for prepro-N/OFQ and NOP receptor in groups of rats that were exposed to differing regimens of social defeat stress. Male Long-Evans rats were exposed to no social defeat, a single, acute social defeat or to repeated social defeats with or witho...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973796</comments>
            <pubDate>Tue, 01 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973796</guid>        </item>
        <item>
            <title>The anorexigenic peptide cocaine-and-amphetamine-regulated transcript modulates rem-sleep in rats</title>
            <link>http://www.medworm.com/index.php?rid=2973795&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000870%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: It is known that the sleep-waking cycle is modulated by several molecules that may also regulate food intake, among them several neuropeptides. The cocaine-and-amphetamine-regulated transcript has been studied in relation to food ingestion, but it seems to have several other functions that may include sleep regulation. In this context, we studied the effect of the intracerebroventricular administration of the cocaine-and-amphetamine-regulated transcript (0.15, 0.3, 0.6, 0.9nmol) on the sleep-waking cycle (12-h recordings), as well as its effect on food intake in rats. Additionally, we analyzed the neuronal activity as measured by c-Fos expression induced by the cocaine-and-amphetamine-regulated transcript in neurons of nuclei involved in the regulation of sleep and feeding behavi...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2973795</comments>
            <pubDate>Tue, 01 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2973795</guid>        </item>
        <item>
            <title>Endogenous peptide: Met-enkephalin-Arg-Phe, differently regulate expression of opioid receptors on chronic treatment</title>
            <link>http://www.medworm.com/index.php?rid=2915951&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000833%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, present study discursively demonstrates that MERF during chronic treatment interacts with all three opioid receptors (μ, δ and κ) in rats and differently regulates their expression. Further, the interaction was such that the induction was mainly observed at molecular/expression level and not at pharmacological level to affect antinociception. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915951</comments>
            <pubDate>Thu, 27 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915951</guid>        </item>
        <item>
            <title>Signaling pathways in PACAP regulation of VIP gene expression in human neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=2915954&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000857%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Ganglia expressing the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) innervate vasoactive intestinal peptide (VIP) containing neurons suggesting a role of PACAP in regulating VIP expression. Human NB-1 neuroblastoma cells were applied to study PACAP regulated VIP gene expression aiming to identify the receptor and the signaling proteins involved. The PACAP receptor subtype PAC1 induced VIP gene expression as (i) PACAP and the PAC1 receptor agonist maxadilan were equally efficient and ∼200-fold more potent than VIP, and (ii) PACAP6-38 and PG99-465, antagonists of PAC1 and VPAC2 receptors, respectively, abolished and did not affect the PACAP-induced VIP mRNA expression, respectively. A pivotal role of PKA was implicated in addition to partial involvement...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915954</comments>
            <pubDate>Wed, 26 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915954</guid>        </item>
        <item>
            <title>Effects of TRH and its analogues on primary cortical neuronal cell damage induced by various excitotoxic, necrotic and apoptotic agents</title>
            <link>http://www.medworm.com/index.php?rid=2915953&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000821%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The tripeptide thyrotropin-releasing hormone (TRH, pGlu-His-Pro-NH2) has been shown to possess neuroprotective activity in in vitro and in vivo models. Since its potential utility is limited by relatively rapid metabolism, metabolically stabilized analogues have been constructed. In the present study we investigated the influence of TRH and its three stable analogues: Montirelin (MON, CG-3703), RGH-2202 (L-6-keto-piperidine-2carbonyl-l-leucyl-l-prolinamide) and Z-TRH (N-carbobenzyloxy-pGlutamyl-Histydyl-Proline) in various models of mouse cortical neuronal cell injury. Twenty four hour pre-treatment with TRH and its analogues in low micromolar concentrations attenuated the neuronal cell death evoked by excitatory amino acids (EAAs: glutamate, NMDA, kainate, quisqualate) and hydro...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915953</comments>
            <pubDate>Sun, 09 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915953</guid>        </item>
        <item>
            <title>Role of NGF in spared DRG following partial dorsal rhizotomy in cats</title>
            <link>http://www.medworm.com/index.php?rid=2915952&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000705%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuroplasticity occurs in the spinal cord in response to lesions, but less is known about the underlying mechanism. This investigation explored the role of intrinsic NGF in axonal sprouting of dorsal root ganglia (DRG) in cats subjected to unilateral removal of L1–L5, L7–S2 DRG, but leaving the L6 DRG (spared DRG) undamaged. The expression of mRNA and protein for NGF and TrkA increased significantly by using in situ hybridization histochemistry and immunohistochemistry. ELISA assay showed that the level of NGF was up-regulated in the spared DRG, compared to the control side. In vitro studies showed that cultured neurons prepared from DRG explants of cats that received partial ganglionectomy had greater neurite growth compared to those prepared from untreated controls, and tha...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915952</comments>
            <pubDate>Thu, 06 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915952</guid>        </item>
        <item>
            <title>The role of β-endorphin in the pathophysiology of major depression</title>
            <link>http://www.medworm.com/index.php?rid=2915950&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000699%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A role for β-endorphin (β-END) in the pathophysiology of major depressive disorder (MDD) is suggested by both animal research and studies examining clinical populations. The major etiological theories of depression include brain regions and neural systems that interact with opioid systems and β-END. Recent preclinical data have demonstrated multiple roles for β-END in the regulation of complex homeostatic and behavioural processes that are affected during a depressive episode. Additionally, β-END inputs to regulatory pathways involving feeding behaviours, motivation, and specific types of motor activity have important implications in defining the biological foundations for specific depressive symptoms. Early research linking β-END to MDD did so in the context of the hypotha...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2915950</comments>
            <pubDate>Sun, 02 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2915950</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=2644975&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000766%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644975</comments>
            <pubDate>Tue, 28 Jul 2009 12:35:36 +0100</pubDate>
            <guid isPermaLink="false">2644975</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2644964&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000730%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644964</comments>
            <pubDate>Tue, 28 Jul 2009 12:35:35 +0100</pubDate>
            <guid isPermaLink="false">2644964</guid>        </item>
        <item>
            <title>Brain derived neurotrophic factor and neurotrophin-4 employ different intracellular pathways to modulate norepinephrine uptake and release in rat hypothalamus</title>
            <link>http://www.medworm.com/index.php?rid=2644967&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000663%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, we showed for the first time that BDNF and NT-4 activate two different intracellular signalling pathways through a Trk B receptor dependent mechanism. Furthermore, present findings support the hypothesis that BDNF and NT-4 acutely applied, could be considered as modulators of noradrenergic transmission and thus may regulate hypothalamic physiological as well as pathophysiological responses. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644967</comments>
            <pubDate>Thu, 02 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644967</guid>        </item>
        <item>
            <title>Norepinephrine regulates arginine vasopressin secretion in hypothalamic paraventricular nucleus relating with pain modulation</title>
            <link>http://www.medworm.com/index.php?rid=2644965&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000687%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Our previous study has pointed that arginine vasopressin (AVP) and norepinephrine (NA) are two most important bioactive substances that play a role in hypothalamic paraventricular nucleus (PVN) regulating pain process. The communication was designed to investigate the interaction between AVP and NA in the rat PVN during the pain process. We used the potassium iontophoresis inducing tail-flick to test the pain threshold, PVN push–pull perfusion to collect the samples, high performance chromatography (HPLC) to determine the NA concentration and radioimmunoassay (RIA) to measure the AVP concentration. The results showed that (1) pain stimulation increased both NA and AVP concentrations in the PVN perfusion liquid; (2) PVN administration of l-glutamate sodium increased AVP, not NA ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644965</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644965</guid>        </item>
        <item>
            <title>Hypothalamic orexin, OX1, αMSH, NPY and MCRs expression in dopaminergic D2R knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=2644966&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000675%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In 5-month-old male and female dopamine receptor 2 (D2R) knockout mice food intake per animal was unaltered while food per g BW was increased. We wished to evaluate the effect of D2R disruption on different components of energy balance and food intake regulation. We determined hypothalamic orexin precursor (PPO) expression, its receptor OX1, serum leptin levels, hypothalamic leptin receptor (OBR), circulating and pituitary α MSH levels, as well as central MC3 and MC4 receptors and NPY mRNA in wildtype and D2R knockout mice (KO).Loss of D2R caused a marked increase in serum prolactin levels, to higher levels in females compared to male KO mice. On the other hand, it produced a female-specific increase in circulating αMSH, and hypothalamic αMSH content, while neurointermediate ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644966</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644966</guid>        </item>
        <item>
            <title>Involvement of neuropeptide Y in the acute, chronic and withdrawal responses of morphine in nociception in neuropathic rats: Behavioral and neuroanatomical correlates</title>
            <link>http://www.medworm.com/index.php?rid=2644970&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000493%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Although morphine is a potent antinociceptive agent, its chronic use developed tolerance in neuropathic pain (NP). Furthermore, opioid antagonist naloxone attenuated the antinociceptive effect of neuropeptide Y (NPY). The present study investigated the role of NPY and NPY Y1/Y5 receptors in acute and chronic actions of morphine in neuropathic rats using thermal paw withdrawal test and immunocytochemistry. In acute study, intracerebroventricular (icv) administration of morphine, NPY or NPY Y1/Y5 receptors agonist [Leu31,Pro34]-NPY produced antinociception, whereas selective NPY Y1 receptors antagonist BIBP3226 caused hyperalgesia. While NPY or [Leu31,Pro34]-NPY potentiated, BIBP3226 attenuated morphine induced antinociception. Chronic icv infusion of morphine via osmotic minipumps...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644970</comments>
            <pubDate>Wed, 24 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644970</guid>        </item>
        <item>
            <title>The role of nitric oxide in the inhibitory effect of ghrelin against penicillin-induced epileptiform activity in rat</title>
            <link>http://www.medworm.com/index.php?rid=2644969&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS014341790900050X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Ghrelin, a gastric peptide with key action on food intake, has been recently recognized as a potential antiepileptic agent. In the present study, we investigated the involvement of nitric oxide in the effect of ghrelin on penicillin-induced epileptiform activity in rat. Thirty minutes after penicillin injection, ghrelin, at doses of 0.5, 1, 2μg, was administered intracerebroventricularly (i.c.v.). Ghrelin, at a dose of 1μg, significantly decreased the mean frequency of epileptiform activity without changing the amplitude whereas other doses of ghrelin (0.5 and 2μg) did not alter either the mean of frequency or amplitude of epileptiform activity. The effects of systemic administration of nitric oxide synthase (NOS) inhibitors, non-selective NG-nitro-l-arginine methyl ester (l-N...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644969</comments>
            <pubDate>Tue, 23 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644969</guid>        </item>
        <item>
            <title>In vivo electrophysiological effects of insulin in the rat brain</title>
            <link>http://www.medworm.com/index.php?rid=2644968&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000511%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Brain insulin has widespread metabolic, neurotrophic, and neuromodulatory functions and is involved in the central regulation of food intake and body weight, learning and memory, neuronal development, neuronal apoptosis, and aging. To understand the neuromodulatory role of insulin, we aimed to characterize its yet undefined in vivo electrophysiological effects. We elected to record from the cerebellar cortex because this region has average insulin concentration and insulin receptor content in relation to the whole brain, and has been previously shown to be a target for insulin signaling. We used in vivo microiontophoresis to apply insulin juxtaneuronally while simultaneously recording changes in spontaneous neuronal activity. The analysis included 553 significant neuronal respons...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644968</comments>
            <pubDate>Sun, 21 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644968</guid>        </item>
        <item>
            <title>Refeeding after prolonged food restriction differentially affects hypothalamic and adipose tissue leptin gene expression</title>
            <link>http://www.medworm.com/index.php?rid=2644972&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000468%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Rat adipose tissue is the principal site of leptin synthesis, however, leptin gene expression has been demonstrated in many rat tissues. Some data indicate that leptin produced by human brain and adipose tissue could cooperate in the regulation of food intake. In this case the regulation of leptin gene expression in hypothalamus and in adipose tissue should be coordinately regulated. Food restriction is often undertaken by many humans trying to lose body weight. Thus, the current study was aimed to analyze whether leptin gene expression in rat hypothalamus and in adipose tissue is regulated synchronously by prolonged food restriction and prolonged food restriction/refeeding.We demonstrate here that although leptin gene is expressed at very low level in rat hypothalamus, its expre...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644972</comments>
            <pubDate>Thu, 18 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644972</guid>        </item>
        <item>
            <title>The human neurokinin B gene, TAC3, and its promoter are regulated by Neuron Restrictive Silencing Factor (NRSF) transcription factor family</title>
            <link>http://www.medworm.com/index.php?rid=2644974&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000481%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We have previously shown that one of the major determinants directing the expression of the preprotachykinin-A (TAC1) gene, which encodes the neuropeptide substance P, is the transcription factor Neuronal Restrictive Silencer Factor (NSRF), which is also termed Repressor Element-1 Silencing Factor (REST). In rodent models of epilepsy, NRSF and its truncated isoform short NRSF (sNRSF), also termed REST4, are increased as an immediate response to seizure. In similar models the neurokinin B (NKB) gene (TAC3) is also induced and NKB has also been shown to be proconvulsant. In this communication we have demonstrated that both the TAC3 endogenous gene and its promoter are regulated, directly or indirectly, by the NRSF transcription factors resulting in both the increased expression of ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644974</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644974</guid>        </item>
        <item>
            <title>RANTES release contributes to the protective action of PACAP38 against sodium nitroprusside in cortical neurons</title>
            <link>http://www.medworm.com/index.php?rid=2644971&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS014341790900047X%2Fabstract%3Frss%3Dyes</link>
            <description>The objective of this study is to determine whether PACAP38 affects expression of regulated on activation normal T expressed and secreted (RANTES) and macrophage inflammatory protein 1-alpha (MIP-1α) in cultured neurons and if these chemokines contribute to the neuroprotective effect of PACAP38. The data show that incubation of neuronal cultures with both PACAP38 and sodium nitroprusside (SNP) reduces the neuronal cell death evoked by SNP alone. PACAP38 dose-dependently increases immunodetectable levels of both RANTES and MIP-1α released in the media by cultured neurons. Co-treatment with a neutralizing antibody to RANTES decreases the PACAP38-mediated protection against SNP. Although RANTES treatment of neurons increased MIP-1α levels in the media and MIP-1α supports neuronal survival...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644971</comments>
            <pubDate>Wed, 03 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644971</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=2463689&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000584%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463689</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463689</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2463679&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000547%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463679</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463679</guid>        </item>
        <item>
            <title>Rapid change of neuropeptide Y levels and gene-expression in the brain of ovariectomized mice after administration of 17β-estradiol</title>
            <link>http://www.medworm.com/index.php?rid=2644973&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000444%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Estrogen alters excitability and changes synaptic morphology in the rat hippocampal formation. We have compared, by means of radioimmunoassay and in situ hybridization, the effects of short-term treatment with 17β-estradiol on neuropeptide Y (NPY) in the brain of ovariectomized mice. A highly significant reduction in concentrations of NPY-like immunoreactivity (LI) was observed in the hippocampal formation, some cortical areas and the caudate nucleus 1h after administration of 17β-estradiol as compared to the control group. In contrast, NPY transcript levels increased in the hippocampal formation (dentate gyrus) and the caudate nucleus, possibly representing a compensatory increase of NPY synthesis following increased estradiol-induced NPY release. These data suggest that 17β-...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2644973</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2644973</guid>        </item>
        <item>
            <title>Activation of orexin signal in basal forebrain facilitates the emergence from sevoflurane anesthesia in rat</title>
            <link>http://www.medworm.com/index.php?rid=2463680&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000456%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Orexinergic system may play an important role in the regulation of anesthesia–arousal. However, which region or which pathway mediated the effect of orexins was still unclear. In current study, we investigated whether activation of orexin signals in basal forebrain (BF) may alter electroencephalographic activity, induction and emergence time to sevoflurane anesthesia in rats. Either orexin-A or orexin-B was injected into the BF while measuring electroencephalogram (EEG) under 1.0 minimum alveolar concentration (2.4%) sevoflurane anesthesia. The induction and emergence time of sevoflurane anesthesia were measured respectively after an injection of orexin receptor agonist (orexin-A or orexin-B) or antagonist (SB-334867A) into the BF also. We found that the administration of orexi...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463680</comments>
            <pubDate>Mon, 25 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463680</guid>        </item>
        <item>
            <title>A novel GalR2-specific peptide agonist</title>
            <link>http://www.medworm.com/index.php?rid=2463681&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000432%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The galanin peptide family and its three receptors have with compelling evidence been implicated in several high-order physiological disorders. The co-localization with other neuromodulators and the distinct up-regulation during and after pathological disturbances has drawn attention to this neuropeptide family. In the current study we present data on receptor binding and functional response for a novel galanin receptor type 2 (GalR2) selective chimeric peptide, M1145 [(RG)2-N-galanin(2-13)-VL-(P)3-(AL)2-A-amide]. The M1145 peptide shows more than 90-fold higher affinity for GalR2 over GalR1 and a 76-fold higher affinity over GalR3. Furthermore, the peptide yields an agonistic effect in vitro, seen as an increase in inositol phosphate (IP) accumulation, both in the absence or the...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463681</comments>
            <pubDate>Thu, 21 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463681</guid>        </item>
        <item>
            <title>Effect of Nociceptin/Orphanin FQ (N/OFQ) and isoflurane on the corticosterone secretory response in mice lacking the N/OFQ prepropeptide (ppN/OFQ-/-)</title>
            <link>http://www.medworm.com/index.php?rid=2463683&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000419%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The effects of subcutaneous Nociceptin/Orphanin FQ (N/OFQ) administration on corticosterone (CORT) secretion were determined in male and female wild-type mice and mice lacking the N/OFQ prepropeptide. Additionally the effect of pretreating animals with isoflurane anesthesia to minimize the potential stress of injection was examined. Although N/OFQ itself did not specifically increase CORT levels in males or females of either genotype, injection alone (either vehicle or N/OFQ) or isoflurane exposure both increased CORT levels in all groups. These results demonstrate that N/OFQ does not elevate circulating CORT levels; however the injection process itself results in increased CORT secretion. Pretreatment with isoflurane did not significantly diminish the CORT response to injection,...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463683</comments>
            <pubDate>Wed, 20 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463683</guid>        </item>
        <item>
            <title>Angiotensin II increases excitability and inhibits a transient potassium current in vagal primary sensory neurons</title>
            <link>http://www.medworm.com/index.php?rid=2463682&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000420%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The octapeptide angiotensin II (ANG II) plays a pivotal role in the maintenance of blood pressure by activating ANG II receptors located in variety of cell types including neurons housed in the central nervous system (CNS) and in the peripheral nervous system (PNS). ANG II (100nM) blocked spike frequency accommodation (SFA) recorded with whole-cell patch technique in acutely isolated nodose ganglion neurons (NGN) from adult rats. ANG II increased the frequency of action potentials (AP) produced by supramaximal 500ms depolarizing currents recorded in both tonic (16Hz vs. 58Hz, control vs. ANG II perfusion respectively, n=9) and phasic (1Hz vs. 38Hz, n=13) NGNs. ANG II produced no significant changes in: the resting membrane potential (−51mV vs. −50mV, n=65), AP overshoot (46mV...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463682</comments>
            <pubDate>Tue, 12 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463682</guid>        </item>
        <item>
            <title>GABA antagonists reverse the somatostatin dependent attenuation of rat locomotor activity</title>
            <link>http://www.medworm.com/index.php?rid=2463684&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000407%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Somatostatin infusion in rat ventral pallidum (VP) led to the attenuation of locomotor activity (Marazioti, A., Kastellakis, A., Antoniou, K., Papasava, D., Thermos, K., 2005. Somatostatin receptors in the ventral pallidum/substantia innominata modulate rat locomotor activity. Psychopharmacology 181, 319–326). In the present study, we investigated the putative circuitry involved in somatostatin’s actions by examining the involvement of GABAergic neurotransmission in locomotor activity subsequent to somatostatin’s infusion into the VP. Male Sprague–Dawley rats, 300–350g, were used for all experiments. Saline or somatostatin (240ng/0.5μl/side) in the absence or presence of bicuculline (GABA-A antagonist; 5mg/kg/ml, i.p.; 120ng/side nucleus accumbens (NAc)) or phaclofen (...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463684</comments>
            <pubDate>Tue, 05 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463684</guid>        </item>
        <item>
            <title>A possible participation of gonadotropin-releasing hormone in the neuroleptic and cataleptic effect of haloperidol</title>
            <link>http://www.medworm.com/index.php?rid=2463688&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000365%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, the studies suggest a possible role of GnRH in the neuroleptic and cataleptic effect of haloperidol. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463688</comments>
            <pubDate>Wed, 29 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463688</guid>        </item>
        <item>
            <title>In vitro characterization of the effects of rat/mouse hemokinin-1 on mouse colonic contractile activity: A comparison with substance P</title>
            <link>http://www.medworm.com/index.php?rid=2463685&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000390%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Rat/mouse hemokinin-1 (r/m HK-1) has been identified as a member of the tachykinin family and its effect in colonic contractile activity remains unknown. We investigated the effects and mechanisms of actions of r/m HK-1 on the mouse colonic contractile activity in vitro by comparing it with that of substance P (SP). R/m HK-1 induced substantial contractions on the circular muscle of mouse colon. The maximal contractile responses to r/m HK-1 varied significantly among proximal-, mid- and distal-colon, suggesting that the action of r/m HK-1 was region-specific in mouse colon. The contractile response induced by r/m HK-1 is primarily via activation of tachykinin NK1 receptors leading to activation of cholinergic excitatory pathways and with a minor contribution of NK2 receptors, whi...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463685</comments>
            <pubDate>Mon, 27 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463685</guid>        </item>
        <item>
            <title>Enkephalin derivative, cyclo[Nε,Nβ-carbonyl-d-Lys2, Dap5] enkephalinamide (cUENK6), induces a highly potent antinociception in rats</title>
            <link>http://www.medworm.com/index.php?rid=2463686&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000389%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The aim of the study was to evaluate whether the newly synthesized analog of enkephalin, cyclo[Nε,Nβ-carbonyl-D-Lys2, Dap5] enkephalinamide (cUENK6), a highly potent μ- (guinea pig ileum assay) and δ-receptors (mouse vas deferens assay) ligand, induces an antinociceptive effect in the hot-plate test and tail-immersion test after intracerebroventricular administration. Our study indicated that this peptide at the dose of 0.25nmol produced comparable but at the dose of 0.5nmol stronger than morphine (13nmol), antinociceptive effect in both tests. Furthermore, rats with developed tolerance to morphine indicated cross-tolerance to antinociceptive effects of cUENK6. The antinociceptive effects of cUENK6 and morphine were inhibited by non-selective opioid receptor antagonist – na...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463686</comments>
            <pubDate>Mon, 20 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463686</guid>        </item>
        <item>
            <title>Effects of the LHRH antagonist Cetrorelix on the brain function in mice</title>
            <link>http://www.medworm.com/index.php?rid=2463687&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000377%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The decapeptide Cetrorelix, an LHRH antagonist, inhibits gonadotropin and sex steroid secretion. Cetrorelix is used for IVF-ET procedures and for the treatment of patients with prostate carcinoma, benign prostatic hyperplasia, endometriosis, leiomyomas and, ovarian cancer. However little is known about the effects of Cetrorelix on the brain function. In the present work the influence of Cetrorelix on different aspects of the brain function was studied following its administration into the lateral brain ventricle in mice. The effects tested included the impairment of the consolidation of a passive avoidance reflex caused by beta-amyloid 25–35, anxiolytic action in the plus-maze, antidepressive action in a forced swimming test and a tail suspension test and open-field behavior. I...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463687</comments>
            <pubDate>Fri, 17 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463687</guid>        </item>
        <item>
            <title>Meetings Calendar</title>
            <link>http://www.medworm.com/index.php?rid=2364546&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000274%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364546</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364546</guid>        </item>
        <item>
            <title>Corrigendum to “PACAP27 regulates ciliary function in primary cultures of rat brain ependymal cells” [Neuropeptides 42 (5–6) (2008) 633–640]</title>
            <link>http://www.medworm.com/index.php?rid=2364545&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417908001327%2Fabstract%3Frss%3Dyes</link>
            <description>The author name: K.S. Mnkkönen should be changed as K.S. Mönkkönen.  The Editorial office regrets the error occurred. (Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364545</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364545</guid>        </item>
        <item>
            <title>Summer neuropeptide conference (snp) stady v meeting (international symposium on signal transduction in health and disease)</title>
            <link>http://www.medworm.com/index.php?rid=2364544&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000183%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364544</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364544</guid>        </item>
        <item>
            <title>Mechanisms operated by endothelin ETA and ETB receptors in the trigeminal ganglion contribute to orofacial thermal hyperalgesia induced by infraorbital nerve constriction in rats</title>
            <link>http://www.medworm.com/index.php?rid=2364543&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417908001297%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Endothelins, acting through specific endothelin ETA and/or ETB receptors, participate in nociceptive processing in models of cancer, inflammatory and neuropathic pain. The present study investigated which cell types express endothelin receptors in the trigeminal ganglion, and the contribution of mechanisms mediated by endothelin ETA and ETB receptors to orofacial heat hyperalgesia induced by unilateral constriction of the infraorbital nerve (CION). Both receptor types were identified by immunohistochemistry in the trigeminal ganglion, ETA receptors on small-sized non-myelinated and myelinated A-fibers and ETB receptors on both satellite glial cells and small-sized non-myelinated neuronal cells. CION promoted ipsilateral orofacial heat hyperalgesia which lasted from Day 2 until Da...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364543</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364543</guid>        </item>
        <item>
            <title>Bone marrow stromal cells attenuate injury-induced changes in galanin, NPY and NPY Y1-receptor expression after a sciatic nerve constriction</title>
            <link>http://www.medworm.com/index.php?rid=2364542&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417908001303%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we have evaluated the effect of MSC administration on the expression of the neuropeptides galanin and NPY, as well as the NPY Y1-receptor (Y1R) in DRG neurons. Animals were subjected to a sciatic nerve SLNC either alone or followed by the administration of MSCs, phosphate-buffered saline (PBS) or bone marrow non-adherent mononuclear cells (BNMCs), directly into the ipsilateral L4 DRG. Seven days after injury, the ipsilateral and contralateral L4–5 DRGs were dissected out and processed for standard immunohistochemistry, using specific antibodies. As previously reported, SLNC induced an ipsilateral increase in the number of galanin and NPY immunoreactive neurons and a decrease in Y1R-positive DRG neurons. The intraganglionic injection of PBS or BNMCs did not modify this patt...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364542</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364542</guid>        </item>
        <item>
            <title>Stress differentially modulates mRNA expression for corticotrophin-releasing hormone receptors in hypothalamus, hippocampus and pituitary of prairie voles</title>
            <link>http://www.medworm.com/index.php?rid=2364541&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417908001315%2Fabstract%3Frss%3Dyes</link>
            <description>This study compares the effect of an acute stressor (restraint for 1h) versus a chronic stressor (social isolation for 4 weeks) on the expression of mRNAs for corticotropin-releasing hormone (CRH), CRH receptor type 1 (CRH-R1) and type 2 (CRH-R2) in the hypothalamus, hippocampus and pituitary of socially monogamous female prairie voles (Microtus ochrogaster). Animals were studied immediately following a stressor or as a function of repairing with a familiar sibling. Despite elevated expression of CRH mRNA, no alteration of CRH-R1 mRNA in the hypothalamus was observed following restraint stress or 4 weeks of social isolation. Hypothalamic CRH-R2 mRNA was significantly lower in voles exposed to restraint or isolation. CRH-R2 mRNA also remained down-regulated in isolated animals when these an...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364541</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364541</guid>        </item>
        <item>
            <title>Nandrolone decanoate administration dose-dependently affects the density of kappa opioid peptide receptors in the rat brain determined by autoradiography</title>
            <link>http://www.medworm.com/index.php?rid=2364540&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417908001339%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The kappa opioid receptor ligand [3H]CI-977 was used to autoradiographically determine the density of kappa opioid receptors in the male rat brain following chronic treatment with the anabolic androgenic steroid nandrolone decanoate at two different doses. As compared to controls, significantly lower densities of the kappa opioid receptor were encountered after two weeks of high dose nandrolone decanoate (15mg/kg) in the nucleus accumbens shell (16%), lateral hypothalamic area (36%), ventromedial hypothalamic nucleus (37%), dorsomedial hypothalamic nucleus (49%), central amygdaloid nucleus, capsular part (28%), lateral globus pallidus (35%) and in the stria terminalis (24%). Furthermore, an up-regulation of the receptor level was observed in the caudate putamen (18%) and in the d...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364540</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364540</guid>        </item>
        <item>
            <title>Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β</title>
            <link>http://www.medworm.com/index.php?rid=2364539&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS014341790900002X%2Fabstract%3Frss%3Dyes</link>
            <description>The objective of the present study was to investigate the role of brain kappa-opioid receptors (KOR) in the antidipsogenic effect promoted by third ventricle injections of interleukin-1β (IL-1β). Wistar male rats were submitted to three different, thirst-inducing, physiological conditions: dehydration induced by water deprivation, hyperosmolarity induced by salt-load and hypovolemia induced by polyethylene glycol subcutaneous injection. Third ventricle injections of IL-1β significantly inhibited the increase in water intake observed in those situations. The pharmacological blockade of central KOR by the selective KOR antagonist nor-binaltorphimine (BNI) at different doses significantly inhibited the antidipsogenic effect induced by the central administration of IL-1β in all conditions ...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364539</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364539</guid>        </item>
        <item>
            <title>Type-1 angiotensin receptors are expressed and transported in motor and sensory axons of rat sciatic nerves</title>
            <link>http://www.medworm.com/index.php?rid=2364538&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000031%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Angiotensin II (Ang II) and its type-1 receptor (AT1) occur in neurons at multiple locations within the organism, but the basic biology of the receptor in the nervous system remains incompletely understood. We previously observed abundant AT1-like binding sites and intense expression of AT1 immunoreactivity in perikarya of the dorsal root ganglion and ventral horn of the rat spinal cord. We have now examined the receptor in rat sciatic nerve, including the dynamics of its axonal transport. Ligand-binding autoradiography of resting nerve showed “hot spots” of 125I-Ang II binding that could be specifically blocked by the AT1 antagonist, losartan. Immunohistochemistry with an AT1-antibody validated by Western blots also showed patches of AT1-reactivity in nerve. These patches we...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364538</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364538</guid>        </item>
        <item>
            <title>Expression of orexin A and its receptor 1 in the choroid plexuses from buffalo brain</title>
            <link>http://www.medworm.com/index.php?rid=2364537&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000195%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the expression of orexin A and OX(1) in the CPs from the brain of an adult mammalian species, Bubalis bubalis, by immunogold-labelling in scanning electron microscopy. Both orexin A and OX(1) immuno-reactivity appeared to be widely distributed on the surface of choroid epithelium. Interestingly, a marked orexin A labelling was detected in the areas surrounding the CP blood capillaries. The expression of prepro-orexin and OX(1) mRNA transcripts of 200 and 300bp, respectively, was assessed in the CPs by reverse-transcription polymerase chain reaction, while Western blotting analysis confirmed the presence of these two proteins in the tissue. Our findings provide the first evidence for orexin A and OX(1) expression in the CPs from mammalian brain, and suggest th...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364537</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2364537</guid>        </item>
        <item>
            <title>Neuronal relationship between orexin-A- and neuropeptide Y-induced orexigenic actions in goldfish</title>
            <link>http://www.medworm.com/index.php?rid=2364536&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000201%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Orexin-induced orexigenic action is mediated by neuropeptide Y (NPY) in goldfish and rodents. A previous study indicated that NPY-induced orexigenic action may also be mediated by orexin-A in goldfish. However, there is little information about the mutual actions of orexin-A and NPY in the goldfish. Therefore, using their specific receptor antagonists, we examined whether the orexigenic actions of orexin-A and NPY mutually interact in the goldfish. The stimulatory effect of intracerebroventricular injection of NPY at 1pmol/g body weight (BW) on food intake was abolished by treatment with the orexin receptor-1 antagonist, SB334867, at 10pmol/g BW whereas the NPY Y1-receptor antagonist, BIBP3226, at 100pmol/g BW attenuated orexin-A (at 2.8pmol/g BW)-stimulated feeding. This led us,...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364536</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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            <title>Calmodulin interacts with PAC1 and VPAC2 receptors and regulates PACAP-induced FOS expression in human neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=2364535&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000213%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) mediates its physiological functions through activation of PAC1, VPAC1 and VPAC2 receptors, and the ubiquitous Ca2+-sensor calmodulin has been implicated in PACAP-induced signaling. The immediate early response gene FOS is a well-known marker of neuronal activation, so we used a human neuroblastoma cell line NB-1 to explore the role of calmodulin in PACAP-induced FOS gene expression. We observed both short-term and prolonged altered PACAP-mediated activation of the FOS gene in the presence of the calmodulin-antagonist W-7. NB-1 cells were shown to express PAC1 and VPAC2 receptors, and immunoprecipitation of both receptors displayed a co-association with calmodulin in the absence of Ca2+. Our findings indi...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364535</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2364534&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000250%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Neuropeptides)</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2364534</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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            <title>Neuroprotective effects of neuropeptide Y-Y2 and Y5 receptor agonists in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2508304&amp;cid=s_38559_168_f&amp;fid=38559&amp;url=http%3A%2F%2Fwww.neuropeptidesjournal.com%2Farticle%2FPIIS0143417909000225%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: It is generally assumed that neurodegeneration is connected with glutamatergic hyperactivity, and that neuropeptide Y (NPY) inhibits glutamate release. Some earlier studies indicated that NPY may have neuroprotective effect; however, the results obtained so far are still divergent, and the role of different Y receptors remains unclear. Therefore in the presented study we investigated the neuroprotective potential of NPY and its Y2, Y5 or Y1 receptor (R) ligands against the kainate (KA)-induced excitotoxicity in neuronal cultures in vitro, as well as in vivo after intrahippocampal KA injection and also in an ischemic middle cerebral artery occlusion model after intraventricular injection of Y2R agonist. NPY compounds were applicated 30min, 1, 3 or 6h after the start of the exposur...</description>
            <author>Neuropeptides</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2508304</comments>
            <pubDate>Wed, 25 Mar 2009 00:00:00 +0100</pubDate>
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