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 'Molecular Pain' source. Mon, 06 Feb 2012 16:52:17 +0100 http://www.medworm.com/index.php?rid=5656509&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F8 Conclusions: Our data show the histological localization of PAF synthases and its receptor in the spinal cord following peripheral nerve injury, and suggest that PAF/PAFr signaling in the spinal cord acts in an autocrine or paracrine manner among the activated microglia and neurons, thus contributing to development of neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5656509 Thu, 02 Feb 2012 05:00:00 +0100 5656509 http://www.medworm.com/index.php?rid=5656510&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F7 Conclusions: These data suggest that the L type Ca2+ channels/NFAT/TRPM8 pathway is a downstream mediator for oxaliplatin-induced cold hyperalgesia, and that Ca2+ channel blockers have prophylactic potential for acute neuropathy. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5656510 Tue, 31 Jan 2012 05:00:00 +0100 5656510 http://www.medworm.com/index.php?rid=5624813&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F6 Conclusions: These results indicate that IL-6 enhances the excitability of dural afferents likely via ERK-mediated modulation of Nav1.7 and these responses contribute to migraine - related pain behavior in vivo. These data provide a cellular mechanism by which IL-6 in the meninges causes sensitization of dural afferents which may contribute to the pathogenesis of migraine headache. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5624813 Tue, 24 Jan 2012 05:00:00 +0100 5624813 http://www.medworm.com/index.php?rid=5624814&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F5 Conclusions: These results highlight the importance of signaling to translation control in peripheral sensitization of nociceptors and provide further evidence for activation of AMPK as a novel treatment avenue for acute and chronic pain states. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5624814 Mon, 23 Jan 2012 05:00:00 +0100 5624814 http://www.medworm.com/index.php?rid=5593112&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F4 Conclusions: We infer from these data that 1) phosphorylation of Akt in the deep dorsal horn is dependent on prior activation of NK1 receptor bearing cells in lamina I, 2) there are parallel spinal intracellular cascades initiated by the carrageenan injection (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5593112 Fri, 13 Jan 2012 05:00:00 +0100 5593112 http://www.medworm.com/index.php?rid=5593114&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F2 Conclusions: Our results demonstrate that IQ blocks the voltage-gated K+ channels to increase AP duration and K2P channels to increase membrane resistance, which are critical for the membrane excitability of DRG neurons. Therefore, we propose that IQ enhances the excitability of DRG neurons by blocking multiple potassium channels and causing pruritus. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5593114 Wed, 11 Jan 2012 05:00:00 +0100 5593114 http://www.medworm.com/index.php?rid=5593113&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F3 Conclusions: Either intranasal or intrathecal pregabalin relieves neuropathic pain behaviours, perhaps due to pregabalin's effect upon anterograde CaValpha2delta-1 protein trafficking from the DRG to the dorsal horn. Intranasal delivery of agents such as pregabalin may be an attractive alternative to systemic therapy for management of neuropathic pain states. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5593113 Wed, 11 Jan 2012 05:00:00 +0100 5593113 http://www.medworm.com/index.php?rid=5593115&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F8%2F1%2F1 Conclusions: We describe proNGF expression by non-neuronal cells over time after nerve injury as well as the association of NGF-responsive fibers to proNGF-expressing target tissues. ProNGF expression increases following nerve injury in those cell types previously suggested to express it. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5593115 Tue, 10 Jan 2012 05:00:00 +0100 5593115 http://www.medworm.com/index.php?rid=5542219&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F102 Oncostatin M (OSM) is a member of the interleukin-6 cytokine family and regulates eg. gene activation, cell survival, proliferation and differentiation. OSM binds to a receptor complex consisting of the ubiquitously expressed signal transducer gp130 and the ligand binding OSM receptor subunit, which is expressed on a specific subset of primary afferent neurons. In the present study, the effect of OSM on heat nociception was investigated in nociceptor-specific gp130 knock-out (SNS-gp130-/-) and gp130 floxed (gp130fl/fl) mice.Subcutaneous injection of pathophysiologically relevant concentrations of OSM into the hind-paw of C57BL6J wild type mice significantly reduced paw withdrawal latencies to heat stimulation. In contrast to gp130fl/fl mice, OSM did not induce heat hypersensitivity in vivo... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5542219 Fri, 23 Dec 2011 05:00:00 +0100 5542219 http://www.medworm.com/index.php?rid=5533467&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F101 Conclusions: The present study demonstrates that rapid S-nitrosylation of actin occurred in vitro in the presence of exogenous NO-generating donors and in vivo in inflammatory pain model mice. Our data suggest that, in addition to the well-known cGMP-dependent protein kinase pathway, S-nitrosylation is involved in pain transmission via disinhibition of inhibitory neurons. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5533467 Thu, 22 Dec 2011 05:00:00 +0100 5533467 http://www.medworm.com/index.php?rid=5533468&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F100 Conclusions Our results suggest that the inducible pan-DRG AvCreERT2 deletor mouse strain is a useful tool to study the role of individual genes in adult sensory neuron function. The pain phenotype of the Cre-induced animal is normal, so that alterations in pain processing can be unambiguously attributed to loss of the targeted gene. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5533468 Wed, 21 Dec 2011 05:00:00 +0100 5533468 http://www.medworm.com/index.php?rid=5533469&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F99 Conclusions: These results suggest spinal PKMzeta is essential for the maintenance of persistent pain by sustaining spinal nociceptive plasticity. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5533469 Tue, 20 Dec 2011 05:00:00 +0100 5533469 http://www.medworm.com/index.php?rid=5520412&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F98 Conclusions: EA and CB2R stimulation reduce inflammatory pain through activation of mu-opioid receptors. EA increases endogenous opioid expression in keratinocytes and infiltrating immune cells at the inflammatory site through CB2R activation. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5520412 Mon, 19 Dec 2011 05:00:00 +0100 5520412 http://www.medworm.com/index.php?rid=5512430&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F97 Conclusions: This is the first evidence of increased D2R mRNA and decreased D2R protein correlated to nociceptive behaviour in a neuropathic model of pain in cg1. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5512430 Thu, 15 Dec 2011 05:00:00 +0100 5512430 http://www.medworm.com/index.php?rid=5512431&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F96 In this study, we present the evidence for the first time, that genetic deletion of PI3Kgamma enhanced scratching behaviours in histamine-dependent and protease -activated receptor 2 (PAR-2)-dependent itch. In contrast, PI3Kgamma-deficient mice did not exhibit enhanced scratching in chloroquine-induced itch, suggesting that PI3Kgamma selectively contributes to certain types of behavioral itch response. Furthermore, PI3Kgamma-deficient mice exhibited normal acute nociceptive responses to thermal and mechanical noxious stimuli. Behavioral licking responses to intraplantar injections of formalin and mechanical allodynia in a chronic inflammatory pain model (CFA) were also not affected by PI3Kgamma gene deletion. Our findings indicate that PI3Kgamma selectively contributes to behavioral itchi... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5512431 Wed, 14 Dec 2011 05:00:00 +0100 5512431 http://www.medworm.com/index.php?rid=5492647&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F95 Conclusions: The central terminals of primary afferents which express high levels of VGluT2-IR but not CGRP-IR terminate mainly in lamina I. The spatial arrangement of VGluT2-IR and CGRP-IR terminals suggest that lamina I neurons receive convergent inputs from presumptive nociceptors that are primarily glutamatergic or peptidergic. This reveals a previously unrecognized level of organization in lamina I consistent with the presence of multiple nociceptive processing pathways. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5492647 Thu, 08 Dec 2011 05:00:00 +0100 5492647 http://www.medworm.com/index.php?rid=5483137&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F94 Conclusions: Our results demonstrate that an elevated level of CGRP in the joint, which is associated with TMD, stimulate neuronal and glial expression of proteins implicated in the development of peripheral and central sensitization. Based on our findings, we propose that inhibition of CGRP-mediated activation of trigeminal neurons and glial cells with selective non-peptide CGRP receptor antagonists would be beneficial in the treatment of TMD. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5483137 Tue, 06 Dec 2011 05:00:00 +0100 5483137 http://www.medworm.com/index.php?rid=5473668&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F92 Conclusion: Our results demonstrate intra- and interfamily phenotypic diversity in pain syndromes produced by a gain-of-function variant of NaV1.7. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5473668 Fri, 02 Dec 2011 05:00:00 +0100 5473668 http://www.medworm.com/index.php?rid=5473667&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F93 This study is the first to provide evidence that gliotransmission contributes to basal mechanical nociception. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5473667 Fri, 02 Dec 2011 05:00:00 +0100 5473667 http://www.medworm.com/index.php?rid=5447666&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F90 Conclusion: These data demonstrate for the first time that kisspeptin regulates pain sensitivity in rodents and suggest that peripheral GPR54 receptors could be targeted by novel drugs in the treatment of inflammatory pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5447666 Wed, 23 Nov 2011 05:00:00 +0100 5447666 http://www.medworm.com/index.php?rid=5447665&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F91 Conclusion: Elevated levels of spinal COX-2 and Egr-1 protein correlate with the presence of pain and hyperalgesia, and may underlie persistent pain, although a direct causal link has still to be established. Understanding the temporal pattern of expression of key mediators in clinical pain states may lead to better strategies to manage pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5447665 Wed, 23 Nov 2011 05:00:00 +0100 5447665 http://www.medworm.com/index.php?rid=5417659&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F88 Background: Clinical studies of osteoarthritis (OA) suggest central sensitization may contribute to the chronic pain experienced. This preclinical study used the monosodium iodoacetate (MIA) model of OA joint pain to investigate the potential contribution of spinal sensitization, in particular spinal glial cell activation, to pain behaviour in this model. Experimental OA was induced in the rat by the intra-articular injection of MIA and pain behaviour (change in weight bearing and distal allodynia) was assessed. Spinal cord microglia (Iba1 staining) and astrocyte (GFAP immunofluorescence) activation were measured at 7, 14 and 28 days post MIA-treatment. The effects of two known inhibitors of glial activation, nimesulide and minocycline, on pain behaviour and activation of microglia and ast... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5417659 Thu, 17 Nov 2011 05:00:00 +0100 5417659 http://www.medworm.com/index.php?rid=5417658&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F89 Conclusions: Our results reveal that a set of novel cannabinoid receptor ligands potently inhibit T-type calcium channels and show analgesic effects in vivo. Our findings suggest possible novel means of mediating pain relief through mixed T-type/cannabinoid receptor ligands. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5417658 Thu, 17 Nov 2011 05:00:00 +0100 5417658 http://www.medworm.com/index.php?rid=5396833&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F87 Conclusions: Our results indicate that the S1 synaptic structures are rapidly destabilized and rearranged following PSL and subsequently stabilized in the maintenance phase of neuropathic pain, suggesting a novel therapeutic target in intractable chronic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5396833 Wed, 09 Nov 2011 05:00:00 +0100 5396833 http://www.medworm.com/index.php?rid=5396834&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F86 Conclusions: These results suggest that PKCzeta, especially PKMzeta isoform, is a significant factor involved in spinal persistent nociceptive processing, specifically, the manifestation of chronic pain states following peripheral inflammation. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5396834 Sat, 05 Nov 2011 04:00:00 +0100 5396834 http://www.medworm.com/index.php?rid=5375464&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F85 Conclusions: These results suggest that the spinal sigma1 receptor system might contribute to diabetic mechanical allodynia and thermal hyperalgesia, which could be potently attenuated by Phe-Phe amide. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5375464 Mon, 31 Oct 2011 04:00:00 +0100 5375464 http://www.medworm.com/index.php?rid=5355405&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F84 Conclusions: Our findings provide evidence that forebrain hyperexcitability confers visceral hyperalgesia, and suppression of central hyperexcitability by activation of KCNQ/M-channel function may provide a therapeutic potential for treatment of abdominal pain syndromes. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5355405 Wed, 26 Oct 2011 04:00:00 +0100 5355405 http://www.medworm.com/index.php?rid=5355407&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F82 The aim of this study was to investigate the expression of prostaglandin EP1 receptor within the ventrolateral periaqueductal grey (VL PAG). The role of VL PAG EP1 receptor in controlling thermonociception and rostral ventromedial medulla (RVM) activity in healthy and neuropathic rats was also examined. EP1 receptor was indeed found to be expressed within the VL PAG and co-localized with vesicular GABA transporter. Intra-VL PAG microinjection of ONO-DI-004, a selective EP1 receptor agonist, dose-dependently reduced tail flick latency as well as respectively increasing and decreasing the spontaneous activity of ON and OFF cells. Furthermore, it increased the ON cell burst and OFF cell pause. Intra-VL PAG prostaglandin E2 (PGE2) behaved similarly to ONO-DI-004. The effects of ONO-DI-004 and ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5355407 Mon, 24 Oct 2011 04:00:00 +0100 5355407 http://www.medworm.com/index.php?rid=5355406&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F83 Autophagy is an intracellular membrane trafficking pathway controlling the delivery of cytoplasmic material to the lysosomes for degradation. It plays an important role in cell homeostasis in both normal settings and abnormal, stressful conditions. It is now recognised that an imbalance in the autophagic process can impact basal cell functions and this has recently been implicated in several human diseases, including neurodegeneration and cancer.Here, we investigated the consequences of nerve injury on the autophagic process in a commonly used model of neuropathic pain. The expression and modulation of the main autophagic marker, the microtubule-associated protein 1 light chain 3 (LC3), was evaluated in the L4-L5 cord segment seven days after spinal nerve ligation (SNL). Levels of LC3-II, ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5355406 Mon, 24 Oct 2011 04:00:00 +0100 5355406 http://www.medworm.com/index.php?rid=5343531&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F81 Conclusions: Blockade of non-evoked pain behaviors but not hypersensitivity suggests differences in the underlying mechanisms of specific components of the pain syndrome and a possibility to individualize aspects of pain management. While it is not known whether the role of p38 MAPK signaling can be expanded to other cancers, the data suggest a need for understanding molecular mechanisms and cellular events that initiate and maintain cancer-induced bone pain for effective management for both ongoing pain as well as breakthrough pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5343531 Thu, 20 Oct 2011 04:00:00 +0100 5343531 http://www.medworm.com/index.php?rid=5330685&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F80 Conclusions: Collectively, our experiments indicate that PAP and NT5E are the main ectonucleotidases that generate adenosine in nociceptive circuits and indicate these enzymes transform pulsatile or sustained nucleotide release into an inhibitory adenosinergic signal. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5330685 Wed, 19 Oct 2011 04:00:00 +0100 5330685 http://www.medworm.com/index.php?rid=5330686&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F79 In this study, we investigated the phenotypes of pain behaviors in PRIP type 1 knockout (PRIP-1-/-) mice. The mutant mice showed hyperalgesic responses in the second phase of the formalin test and the von Frey test as compared with those in wild-type mice. In situ hybridization studies of GABAA receptors revealed significantly decreased expression of gamma2 subunit mRNA in the dorsal and ventral horns of the spinal cord in PRIP-1-/- mice, but no difference in alpha1 subunit mRNA expression. beta2 subunit mRNA expression was significantly higher in PRIP-1-/- mice than in wild-type mice in all areas of the spinal cord. Patch-clamp recordings showed that the baseline shift tended to be smaller in PRIP-1-/- mice than in wild-type mice, although this was not statistically significant. The slow ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5330686 Tue, 18 Oct 2011 04:00:00 +0100 5330686 http://www.medworm.com/index.php?rid=5292958&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F78 Conclusion: Our results show that the sEH can regulate mechanical hyperalgesia during inflammation by inactivating 8,9-EET, which sensitizes TRPA1 expressing nociceptors. Therefore we suggest that influencing the CYP450 pathway, which is actually highly considered to treat cardiovascular diseases, may cause pain side effects. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5292958 Tue, 04 Oct 2011 04:00:00 +0100 5292958 http://www.medworm.com/index.php?rid=5268671&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F76 Conclusions: These results show that most dynorphin-expressing cells in the superficial dorsal horn are inhibitory interneurons, and that they largely correspond to the population that is defined by the presence of galanin. We estimate that dynorphin is present in ~32% of inhibitory interneurons in lamina I and 11% of those in lamina II. Since the proportion of GABAergic boutons that contain PPD in these laminae was considerably lower than this, our findings suggest that these neurons may generate relatively small axonal arborisations. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5268671 Thu, 29 Sep 2011 04:00:00 +0100 5268671 http://www.medworm.com/index.php?rid=5268670&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F77 Conclusions: The more abundant lipid raft compartment of knock-in neurons was enriched in P2X3 receptors that exhibited stronger functional responses. These results suggest that the membrane microenvironment of trigeminal sensory neurons is an important factor in determining sensitization of P2X3 receptors and could contribute to a migraine phenotype by enhancing ATP-mediated responses (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5268670 Thu, 29 Sep 2011 04:00:00 +0100 5268670 http://www.medworm.com/index.php?rid=5268673&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F74 Conclusions: Our data show that TLR2 contributes to nerve injury-induced proinflammatory chemokine/cytokine gene expression and macrophage infiltration in the DRG, which may have relevance in the reduced pain hypersensitivity in TLR2 knock-out mice after spinal nerve injury. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5268673 Wed, 28 Sep 2011 04:00:00 +0100 5268673 http://www.medworm.com/index.php?rid=5268672&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F75 Conclusions: The present findings suggest that peripheral Glu receptor mechanisms may contribute to cold hyperalgesia in the tongue but not in the facial skin, and also contribute to heat hyperalgesia in the tongue and facial skin, and that the mitogen-activated protein kinase cascade in Vc-C2 neurons may be involved in these Glu-evoked hyperalgesic effects. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5268672 Wed, 28 Sep 2011 04:00:00 +0100 5268672 http://www.medworm.com/index.php?rid=5268674&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F73 Tenderness and mechanical allodynia are key symptoms of malignant tumor, inflammation and neuropathy. The proinflammatory cytokine interleukin-6 (IL-6) is causally involved in all three pathologies. IL-6 not only regulates innate immunity and inflammation but also causes nociceptor sensitization and hyperalgesia. In general and in most cell types including immune cells and sensory neurons, IL-6 binds soluble receptor subunits which heteromerize with membrane bound IL-6 signal transducer gp130. In the present study, we used a conditional knock-out strategy to investigate the importance of signal transducer gp130 expressed in C nociceptors for the generation and maintenance of mechanical hypersensitivity. Nociceptors were sensitized to mechanical stimuli by experimental tumor and this nocice... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5268674 Tue, 27 Sep 2011 04:00:00 +0100 5268674 http://www.medworm.com/index.php?rid=5257301&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F72 In our earlier study, noradrenaline (NA) stimulated ATP release from dorsal root ganglion (DRG) neurons as mediated via beta3 adrenoceptors linked to Gs protein involving protein kinase A (PKA) activation, to cause allodynia. The present study was conducted to understand how ATP is released from DRG neurons. In an outside-out patch-clamp configuration from acutely dissociated rat DRG neurons, single-channel currents, sensitive to the P2X receptor inhibitor PPADS, were evoked by approaching the patch-electrode tip close to a neuron, indicating that ATP is released from DRG neurons, to activate P2X receptor. NA increased the frequency of the single-channel events, but such NA effect was not found for DRG neurons transfected with the siRNA to silence the cystic fibrosis transmembrane conducta... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5257301 Sat, 24 Sep 2011 04:00:00 +0100 5257301 http://www.medworm.com/index.php?rid=5246362&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F68 Conclusions: The activation of spinal ERK, p38 and CaMKII, alongside nNOS, is involved in chronic morphine-induced CGRP up-regulation in both the DRG and SCDH. Moreover, the stimulation of CaMKII in the DRG likely directly regulates the expression of CGRP associated with morphine analgesic tolerance. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5246362 Wed, 21 Sep 2011 04:00:00 +0100 5246362 http://www.medworm.com/index.php?rid=5246361&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F69 Conclusions: These results suggest that the repetitive intrathecal administration of antidepressants permanently cures ICS-induced FM pain in mice. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5246361 Wed, 21 Sep 2011 04:00:00 +0100 5246361 http://www.medworm.com/index.php?rid=5246360&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F70 Neuropathic pain is a debilitating clinical condition with few efficacious treatments, warranting development of novel therapeutics. We hypothesized that dysregulated translation regulation pathways may underlie neuropathic pain. Peripheral nerve injury induced reorganization of translation machinery in the peripheral nervous system of rats and mice, including enhanced mTOR and ERK activity, increased phosphorylation of mTOR and ERK downstream targets, augmented eIF4F complex formation and enhanced nascent protein synthesis. The AMP activated protein kinase (AMPK) activators, metformin and A769662, inhibited translation regulation signaling pathways, eIF4F complex formation, nascent protein synthesis in injured nerves and sodium channel-dependent excitability of sensory neurons resulting i... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5246360 Wed, 21 Sep 2011 04:00:00 +0100 5246360 http://www.medworm.com/index.php?rid=5246359&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F71 Conclusions: Supported by current understanding of basal ganglia role in pain processing, the findings suggest a significant role of the basal ganglia in the pathophysiology of the episodic migraine. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5246359 Wed, 21 Sep 2011 04:00:00 +0100 5246359 http://www.medworm.com/index.php?rid=5217698&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F67 Conclusions: Overall, lamina I/II neurons express a unique combination of functional sodium channels that are highly divergent from the sodium channel isoforms found within peripheral nociceptors, creating potentially complementary or distinct ion channel targets for future pain therapeutics. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5217698 Mon, 12 Sep 2011 04:00:00 +0100 5217698 http://www.medworm.com/index.php?rid=5217699&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F66 Progress in the somatosensory field has been restricted by the limited number of genetic tools available to study gene function in peripheral sensory neurons. Here we generated a Cre-driver mouse line that expresses Cre-recombinase from the locus of the sensory neuron specific gene Advillin. These mice displayed almost exclusive Cre-mediated recombination in all peripheral sensory neurons. As such, the Advillin-Cre-driver line will be a powerful tool for targeting peripheral neurons in future investigations. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5217699 Sun, 11 Sep 2011 04:00:00 +0100 5217699 http://www.medworm.com/index.php?rid=5168898&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F65 Conclusions: This study provides the first evidence that DNA methylation of a single gene plays a role in chronic pain in humans and animal models. This has important implications for understanding the mechanisms involved in chronic pain and for pain therapy. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5168898 Wed, 24 Aug 2011 23:00:00 +0100 5168898 http://www.medworm.com/index.php?rid=5155687&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F64 Conclusion: This study demonstrated the collective contribution of medial and lateral pathway neurons to the noxious intensity coding. Additionally, we provide evidence that ensemble spike count may be the most reliable method for coding pain intensity in the brain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155687 Tue, 23 Aug 2011 23:00:00 +0100 5155687 http://www.medworm.com/index.php?rid=5155689&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F62 Conclusions: The structural determinants involved in activation of TRPA1 by LAs are disparate from those involved in activation by menthol or those involved in activation of TRPV1 by LAs. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155689 Mon, 22 Aug 2011 23:00:00 +0100 5155689 http://www.medworm.com/index.php?rid=5155688&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F63 Conclusion: VSV-G pseudotyped lentivectors containing the human elongation factor 1alpha (EF1alpha)-EGFP expression cassette demonstrated relatively efficient transduction to sensory neurons following direct injection into the DRG. These results clearly show the potential of lentivectors as a viable system for delivering target genes into DRGs to explore basic mechanisms of neuropathic pain, with the potential for future clinical use in treating chronic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155688 Mon, 22 Aug 2011 23:00:00 +0100 5155688 http://www.medworm.com/index.php?rid=5155690&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F61 Acupuncture and electro-acupuncture (EA) are now widely used to treat disorders like pain. We and others have shown previously that current frequency, intensity and treatment duration all significantly influence the anti-nociceptive effects of EA. There is evidence that stimulating sites also affect the antinociception, with EA applied ipsilaterally to the pain site being more effective under some pain states but contralateral EA under others. It was recently reported that local adenosine A1 receptors were responsible for ipsilateral acupuncture, but what mechanisms specifically mediate the anti-nociceptive effects of contralateral acupuncture or EA remains unclear. In the present study, we applied 100 Hz EA on the ipsi- or contra-lateral side of rats with inflammatory pain induced by intr... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155690 Sun, 21 Aug 2011 23:00:00 +0100 5155690 http://www.medworm.com/index.php?rid=5155691&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F60 Conclusions: These results indicate that a large enhancement of P2X3 receptor activity and an increase in the membrane expression of P2X3 receptors contribute to the development of chronic pain in STZ-induced diabetic rats and suggest a possible target for the treatment of diabetic neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155691 Wed, 17 Aug 2011 23:00:00 +0100 5155691 http://www.medworm.com/index.php?rid=5155692&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F59 Cellular prion protein (PrPC) inhibits N-Methyl-D-Aspartate (NMDA) receptors. Since NMDA receptors play an important role in the transmission of pain signals in the dorsal horn of spinal cord, we thus wanted to determine if PrPC null mice show a reduced threshold for various pain behaviours.We compared nociceptive thresholds between wild type and PrPC null mice in models of inflammatory and neuropathic pain, in the presence and the absence of a NMDA receptor antagonist.2-3 months old male PrPC null mice exhibited an MK-801 sensitive decrease in the paw withdrawal threshold in response both mechanical and thermal stimuli. PrPC null mice also exhibited significantly longer licking/biting time during both the first and second phases of formalin-induced inflammation of the paw, which was again... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5155692 Mon, 15 Aug 2011 23:00:00 +0100 5155692 http://www.medworm.com/index.php?rid=5129945&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F58 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5129945 Sat, 13 Aug 2011 23:00:00 +0100 5129945 http://www.medworm.com/index.php?rid=5102771&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F57 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5102771 Thu, 04 Aug 2011 23:00:00 +0100 5102771 http://www.medworm.com/index.php?rid=5094310&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F56 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5094310 Wed, 03 Aug 2011 23:00:00 +0100 5094310 http://www.medworm.com/index.php?rid=5076400&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F55 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5076400 Thu, 28 Jul 2011 23:00:00 +0100 5076400 http://www.medworm.com/index.php?rid=5076401&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F54 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5076401 Wed, 27 Jul 2011 23:00:00 +0100 5076401 http://www.medworm.com/index.php?rid=5076403&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F52 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5076403 Tue, 26 Jul 2011 23:00:00 +0100 5076403 http://www.medworm.com/index.php?rid=5076402&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F53 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5076402 Tue, 26 Jul 2011 23:00:00 +0100 5076402 http://www.medworm.com/index.php?rid=5048332&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F51 ${item.shortDescription} (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5048332 Wed, 20 Jul 2011 23:00:00 +0100 5048332 http://www.medworm.com/index.php?rid=5026855&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F50 Conclusions: Our results provide evidence that the NOS/NO pathway contributes to behavioral pain responses evoked by tissue injury and nerve injury. In particular, nNOS may be important for spinal microglial activation and tactile allodynia after nerve injury. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5026855 Wed, 13 Jul 2011 23:00:00 +0100 5026855 http://www.medworm.com/index.php?rid=5006362&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F49 Conclusions: We demonstrate here that resveratrol regulates p35 promoter activity in PC12 cells and DRG neurons. Most importantly, resveratrol blocks the TNF-alpha-mediated increase in p35 promoter activity, thereby reducing p35 expression and subsequent Cdk5 kinase activity. This new molecular mechanism adds to the known analgesic effects of resveratrol and confirms the need for identifying new analgesics based on their ability to inhibit Cdk5 activity for effective treatment of pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5006362 Wed, 06 Jul 2011 23:00:00 +0100 5006362 http://www.medworm.com/index.php?rid=4967611&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F47 Itch sensation is one of the major sensory experiences of human and animals. Recent studies have proposed that gastrin releasing peptide (GRP) is a key neurotransmitter for itch in spinal cord. However, no direct evidence is available to indicate that GRP actually mediate responses between primary afferent fibers and dorsal horn neurons. Here we performed integrative neurobiological experiments to test this question. We found that a small population of rat dorsal horn neurons responded to GRP application with increases in calcium signaling. Whole-cell patch-clamp recordings revealed that a part of superficial dorsal horn neurons responded to GRP application with the increase of action potential firing in adult rats and mice, and these dorsal horn neurons received exclusively primary affere... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4967611 Thu, 23 Jun 2011 23:00:00 +0100 4967611 http://www.medworm.com/index.php?rid=4910407&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F46 Conclusions: Our findings suggest that central NMDA receptor NR2 subunits play an important role in the central processing of trigeminal neuralgia-like nociception in rats with compression of the trigeminal nerve root. Our data further indicate that the targeted blockade of NR2 subunits is a potentially important new treatments strategy for trigeminal neuralgia-like nociception. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4910407 Tue, 07 Jun 2011 23:00:00 +0100 4910407 http://www.medworm.com/index.php?rid=4910408&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F45 Conclusion: Intensities of EA plays an important role in modulating central pain perception. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4910408 Mon, 06 Jun 2011 23:00:00 +0100 4910408 http://www.medworm.com/index.php?rid=4901303&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F44 Conclusion: Based on these studies, we now propose a model of TRPV1 expression that is dependent on Sp1-like transcription factors with Sp4 playing a predominant role in activating TRPV1 RNA transcription in DRG neurons. Given that increases of TRPV1 expression have been implicated in a wide range of pathophysiologic states including persistent painful conditions, blockade of Sp1-like transcription factors represents a novel direction in therapeutic strategies. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4901303 Sun, 05 Jun 2011 23:00:00 +0100 4901303 http://www.medworm.com/index.php?rid=4901304&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F43 Conclusions: RT might be important in nociception of the mouse. In addition, we showed an important role of Cav3.2 subtype of T-channel in RT burst firing pattern. The decreased occurrence and slowing of the bursts in RT neurons might cause the increased VP bursts. These changes would be factors contributing to alternation of pain behavior in the Cav3.2 KO mice. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4901304 Fri, 03 Jun 2011 23:00:00 +0100 4901304 http://www.medworm.com/index.php?rid=4891614&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F42 Conclusion: The results suggest that lumbar dural mast cells may be sufficient but are not necessary for capsaicin or carrageenan-induced hyperalgesia. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4891614 Thu, 02 Jun 2011 23:00:00 +0100 4891614 http://www.medworm.com/index.php?rid=4870718&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F41 Conclusions: These findings that a short-term application of artemin inhibits the TRPA1 channel's activity and the sequential pain behaviors suggest a role of artemin in regulation of sensory neurons. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4870718 Thu, 26 May 2011 23:00:00 +0100 4870718 http://www.medworm.com/index.php?rid=5017853&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F40 Conclusions: Our results indicate that TNFα in the spinal cord and the DRG are involved in neuropathic pain, following the peripheral HIV gp120 application, and that blockade of the glial product TNFα reverses neuropathic pain induced by HIV gp120 application. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=5017853 Thu, 19 May 2011 23:00:00 +0100 5017853 http://www.medworm.com/index.php?rid=4847251&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F40 Conclusions: Our results indicate that spinal astrocytes activation is involved in neuropathic pain, following the peripheral HIV gp120 application, and that blockade of the glial product TNFalpha reversed neuropathic pain induced by HIV gp120 (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4847251 Thu, 19 May 2011 23:00:00 +0100 4847251 http://www.medworm.com/index.php?rid=4839739&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F38 Conclusions: The results show that Homer1a expressed in forebrain neurons, prevents the development of pain hypersensitivity in arthritis and disrupts pain-related plasticity at synapses in amygdaloid nuclei. Furthermore, Homer1a eliminates the effect of an mGluR1 antagonist, which is consistent with the well-documented disruption of mGluR1 signaling by Homer1a. These findings emphasize the important role of mGluR1 in pain-related amygdala plasticity and provide evidence for the involvement of Homer1 proteins in the forebrain in the modulation of pain hypersensitivity. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4839739 Wed, 18 May 2011 23:00:00 +0100 4839739 http://www.medworm.com/index.php?rid=4839740&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F37 Conclusions: Our results support the notion that TRPV3 and TRPV4 likely make limited and strain-dependent contributions to innocuous warm temperature perception or noxious heat sensation, even when TRPV1 is masked. These findings imply the existence of other significant mechanisms for heat perception. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4839740 Mon, 16 May 2011 23:00:00 +0100 4839740 http://www.medworm.com/index.php?rid=4827630&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F36 Conclusions: These results show that galanin, NPY, nNOS and parvalbumin can be used to define four distinct neurochemical populations of inhibitory interneurons. Together with results of a recent study, they suggest that the galanin and NPY populations account for around half of the inhibitory interneurons in lamina I and a quarter of those in lamina II. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4827630 Sat, 14 May 2011 23:00:00 +0100 4827630 http://www.medworm.com/index.php?rid=4827633&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F33 Conclusions: Our results suggest that cPA and its stable analog 2ccPA inhibit chronic and acute inflammation-induced C-fiber stimulation, and that the central effects of 2ccPA following repeated treatments attenuate neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4827633 Fri, 13 May 2011 23:00:00 +0100 4827633 http://www.medworm.com/index.php?rid=4827632&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F34 Conclusions: The results from these studies indicate that calcium/calmodulin interferes with the association of AKAP150 with TRPV1, potentially extending resensitization of the channel. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4827632 Fri, 13 May 2011 23:00:00 +0100 4827632 http://www.medworm.com/index.php?rid=4827631&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F35 Conclusion: This systematic study clearly demonstrates that activation of KATP could have significant modulatory effects on the excitability of sensory neurons and thus on sensory behaviors, such as nociception. KATP activators can be evaluated clinically for the treatment of pain symptoms. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4827631 Fri, 13 May 2011 23:00:00 +0100 4827631 http://www.medworm.com/index.php?rid=4811968&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F32 Conclusions: Our data show that Nav1.7 is the dominant sodium channel in rat and mouse OSN, and may explain anosmia in Nav1.7 null mouse and patients with Nav1.7-related CIP. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4811968 Mon, 09 May 2011 23:00:00 +0100 4811968 http://www.medworm.com/index.php?rid=4801623&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F31 Conclusion: These results demonstrate that sensitization of bladder afferents induced by inflammation is partly suppressed by intravesical activation of cannabinoid receptors, an effect that appears to be mediated by CB1 receptors. Also, TRPV1 positive fibers were found to co-express CB1, supporting the hypothesis of a direct action of the cannabinoid agonist on nociceptive afferents. Taken together, these results indicate a peripheral modulation by the cannabinoid system of bladder hypersensitivity during inflammation. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4801623 Sun, 08 May 2011 23:00:00 +0100 4801623 http://www.medworm.com/index.php?rid=4762224&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F30 Conclusions: In summary, our results clearly support an important role of TRESK channels in determining neuronal excitability in specific DRG neurons subpopulations, and show that axonal injury down-regulates TRESK channels, therefore contributing to neuronal hyperexcitability. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4762224 Wed, 27 Apr 2011 23:00:00 +0100 4762224 http://www.medworm.com/index.php?rid=4752949&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F29 Conclusions: Our findings demonstrate that chronic treatment with oxaliplatin produces neurotoxic changes in BALB/c mice, confirming that this model is a suitable tool to conduct further mechanistic studies of oxaliplatin-related antineoplastic activity, peripheral neurotoxicity and pain. Further, this model can be used for the preclinical discovery of new neuroprotective and analgesic compounds.KEYWORDS: Oxaliplatin, peripheral neuropathy, cold hyperalgesia, mechanical allodynia, dorsal rootganglia, spinal dorsal horn, electrophysiology. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4752949 Mon, 25 Apr 2011 23:00:00 +0100 4752949 http://www.medworm.com/index.php?rid=4732659&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F28 Conclusions: We suggest that for studying heterotopic nociceptive facilitation the evoked brain response is suitable and relevant for investigating plasticity at the level of the brain and is perhaps a more sensitive and reliable marker than the perceived pain intensity (e.g. VAS). (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4732659 Tue, 19 Apr 2011 23:00:00 +0100 4732659 http://www.medworm.com/index.php?rid=4722973&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F26 Conclusions: These findings are consistent with the hypothesis that the high level of endogenous galanin in injured primary afferents activates peripheral GalR2, which leads to an increase in C-fibre mechanical activation thresholds and a marked reduction in evoked and ongoing nociceptive responses. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4722973 Fri, 15 Apr 2011 23:00:00 +0100 4722973 http://www.medworm.com/index.php?rid=4703593&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F23 Conclusions: The present study demonstrated the abolition of the thermal, mechanical, and somatic chemical antinociceptive effects of (-)-pentazocine and retention of the visceral chemical antinociceptive effects of (-)-pentazocine in MOP-KO mice. These results suggest that the MOP receptor plays a pivotal role in thermal, mechanical, and somatic chemical antinociception induced by (-)-pentazocine, whereas the KOP receptor is involved in visceral chemical antinociception induced by (-)-pentazocine. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4703593 Sat, 09 Apr 2011 23:00:00 +0100 4703593 http://www.medworm.com/index.php?rid=4657913&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F21 Conclusion: Taken together, the present results suggest that 5-HIAA plays an important role in modulating peripheral thermal hyperalgesia in CFA induced inflammation, probably via a non-serotonin receptor mechanism. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4657913 Tue, 29 Mar 2011 23:00:00 +0100 4657913 http://www.medworm.com/index.php?rid=4652007&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F20 Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesi... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4652007 Sun, 27 Mar 2011 23:00:00 +0100 4652007 http://www.medworm.com/index.php?rid=4626201&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F19 Conclusions: This study provided an integrated view to explore the functional specificity of acupuncture, in which both needling sensation and the following neural cascades may contribute to the overall effect of acupuncture through dynamic reconfiguration of complex neural networks. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4626201 Wed, 23 Mar 2011 00:00:00 +0100 4626201 http://www.medworm.com/index.php?rid=4621471&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F18 Conclusions: Psychophysical and electrophysiological data were consistent with the ability of short high intensity infrared laser pulses to selectively produce A-delta mediated pain and of longer pulses to selectively produce C fiber mediated thermal pain. Thus, the use of these or similar protocols may be useful in developing and testing novel therapeutics based on the differential molecular mechanisms underlying activation of the two fiber types (e.g., TRPV1, TRPV2, etc). In addition, these protocol may be useful in determining the fiber mediation of different clinical pain types which may, in turn be useful in treatment choice. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4621471 Tue, 22 Mar 2011 00:00:00 +0100 4621471 http://www.medworm.com/index.php?rid=4559359&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F17 Conclusions: Our results indicate that miRNAs may participate in the regulatory mechanisms of genes associated with the pathophysiology of chronic pain as well as the nociceptive processing following acute noxious stimulation. We found substantial evidence that miRNAs are differentially regulated in DRG and the dorsal horn of the spinal cord under different pain states. Therefore, miRNA expression in the nociceptive system shows not only temporal and spatial specificity but is also stimulus-dependent. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4559359 Mon, 07 Mar 2011 00:00:00 +0100 4559359 http://www.medworm.com/index.php?rid=4511657&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F16 In this report, we describe the expression and distribution of voltage-gated sodium channels in the dorsal root ganglion. We also review evidence regarding changes in their expression under neuropathic pain conditions and their roles in behavioral responses in a variety of neuropathic pain models. We finally discuss their potential involvement in neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4511657 Wed, 23 Feb 2011 00:00:00 +0100 4511657 http://www.medworm.com/index.php?rid=4506715&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F15 Conclusions: These results suggest a probable "TLR3-astrocytes-IL-1/MCP-1" pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4506715 Tue, 22 Feb 2011 00:00:00 +0100 4506715 http://www.medworm.com/index.php?rid=4464057&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F14 Conclusion: Neuropathic injury causes primary sensory neurons to become hyperexcitable to ATP-evoked P2X receptor-mediated depolarization, a phenotypic switch sensitive to PKC modulation and mediated by increased activity of TTX-sensitive VGSCs. Upregulation in VGSC activity after injury is likely mediated by increased expression of the Nav1.3 subunit, and the function of the Nav1.3 channel is regulated by PKC. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4464057 Fri, 11 Feb 2011 00:00:00 +0100 4464057 http://www.medworm.com/index.php?rid=4459249&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F12 Conclusions: The present findings have demonstrated that mechanical allodynia and thermal hyperalgesia occur in the lateral facial skin after CNX and also suggest that ERK phosphorylation of Vc and C1-C2 neurons and astroglial cell activation are involved in orofacial extraterritorial pain following cervical nerve injury. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4459249 Thu, 10 Feb 2011 00:00:00 +0100 4459249 http://www.medworm.com/index.php?rid=4459248&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F13 Conclusions: These results strongly suggest that P2Y1 is required for normal thermal signaling in cutaneous sensory afferents. Furthermore, they suggest that nucleotides released from peripheral tissues play a critical role in the transduction of thermal stimuli in some fiber types. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4459248 Thu, 10 Feb 2011 00:00:00 +0100 4459248 http://www.medworm.com/index.php?rid=4432707&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F11 In this study, we report that PICK1 is expressed in neurons of the dorsal root ganglion (DRG) and spinal cord dorsal horn, two major pain-related regions. PICK1 was present in approximately 29.7% of DRG neurons, most of which were small--less than 750 um2 in cross-sectional area. Some of these PICK-1-positive cells co-labeled with isolectin B4 or calcitonin-gene-related peptide. In the dorsal horn, PICK1 immunoreactivity was concentrated in the superficial dorsal horn, where it was prominent in the postsynaptic density, axons, and dendrites. Targeted disruption of PICK1 gene did not affect basal paw withdrawal responses to acute noxious thermal and mechanical stimuli or locomotor reflex activity, but it completely blocked the induction of peripheral nerve injury-induced mechanical and ther... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4432707 Thu, 03 Feb 2011 00:00:00 +0100 4432707 http://www.medworm.com/index.php?rid=4393632&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F10 Conclusions: To our knowledge, this is the first report of an ASIC-current inhibitor derived of a marine-plant extract, and in a phenolic compound. The antinociceptive effects of BM-21 and thalassiolin B may be partially because of this action on the ASICs. That the active components of the extract are able to cross the blood-brain barrier gives them an additional advantage for future uses as tools to study pain mechanisms with a potential therapeutic application. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4393632 Mon, 24 Jan 2011 00:00:00 +0100 4393632 http://www.medworm.com/index.php?rid=4382013&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F9 Conclusion: The identification of the rat exon 11 and its associated variants further demonstrated conservation of 5' splicing in OPRM1 genes among rodents and humans. The functional relevance of these exon 11 associated variants was suggested by the region-specific expression of their mRNAs and the influence of the N-terminal sequence on agonist-induced G protein coupling in the novel N-terminal variant, rMOR-1H2. The importance of the exon 11-associated variants in mice in M6G and heroin analgesia revealed in the exon 11 knockout mouse implies that these analogous rat variants may also play similar roles in rat. The complexity created by alternative splicing of the rat OPRM1 gene may provide important insights of understanding the diverse responses to the various mu opioids seen in rats.... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4382013 Fri, 21 Jan 2011 00:00:00 +0100 4382013 http://www.medworm.com/index.php?rid=4376992&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F8 Conclusion: These results indicated that spinal NR2B-containing NMDA receptors are involved in the oxaliplatin-induced mechanical allodynia. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4376992 Thu, 20 Jan 2011 00:00:00 +0100 4376992 http://www.medworm.com/index.php?rid=4360282&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F7 Conclusion: These data suggest a possible involvement of endovanilloids in the cortical plastic changes associated with peripheral nerve injury and indicate that therapies able to normalize endovanilloid transmission may prove useful in ameliorating the symptoms and central sequelae associated with neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4360282 Mon, 17 Jan 2011 00:00:00 +0100 4360282 http://www.medworm.com/index.php?rid=4349033&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F6 In this study we used mGlu2 or mGlu3 knock-out mice to dissect the specific role for these two receptors in the endogenous control of inflammatory pain and their specific contribution to the analgesic activity of mixed mGlu2/3 receptor agonists.Our results showed that mGlu2-/- mice display a significantly greater pain response compared to their wild type littermates. Interestingly the increased pain sensitivity in mGlu2-/- mice occurred only in the second phase of the formalin test. No differences were observed in the first phase. In contrast, mGlu3-/- mice did not significantly differ from their wild type littermates in either phase of the formalin test.When systemically injected, a single administration of the mGlu2/3 agonist, LY379268 (3 mg/kg, ip), showed a significant reduction of bot... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4349033 Fri, 14 Jan 2011 00:00:00 +0100 4349033 http://www.medworm.com/index.php?rid=4445184&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F3 The aim of this study was to obtain evidences of a possible analgesic role for palmitoylethanolamide (PEA) in chronic granulomatous inflammation sustained by mast cell (MC) activation in rats at 96 hours. PEA (200-400-800 μg/mL), locally administered at time 0, reduced in a concentration-dependent manner the expression and release of NGF in comparison with saline-treated controls. PEA prevented nerve formation and sprouting, as shown by histological analysis, reduced mechanical allodynia, evaluated by Von Frey filaments, and inhibited dorsal root ganglia activation. These results were supported by the evidence that MCs in granuloma were mainly degranulated and closely localized near nerve fibres and PEA significantly reduced MC degranulation and nerves fibre formation. These findings are ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4445184 Mon, 10 Jan 2011 00:00:00 +0100 4445184 http://www.medworm.com/index.php?rid=4330276&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F3 The aim of this study was to obtain evidence of a possible analgesic role for palmitoylethanolamide (PEA) in chronic granulomatous inflammation sustained by mast cell (MC) activation in rats at 96 hours. PEA (200-400-800ug/mL), locally administered at time 0 reduced in a concentration-dependent manner the expression and release of NGF in comparison with saline-treated controls. PEA prevented nerve formation and sprouting, as shown by histological analysis, reduced mechanical allodynia, evaluated by Von Frey filaments, and inhibited dorsal root ganglia activation. These results were supported by the evidence that MCs in granuloma were mainly degranulated and closely localized near nerve fibres and PEA significantly reduced MC degranulation and nerves fibre formation. These findings are the ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4330276 Mon, 10 Jan 2011 00:00:00 +0100 4330276 http://www.medworm.com/index.php?rid=4330275&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F4 Conclusions: These data demonstrate that inflammation induces both ongoing pain and evoked hypersensitivity that can be differentiated on the basis of time course. Ongoing pain (a) is transient, (b) driven by peripheral input resulting from the injury, (c) dependent on TRPV1 positive fibers and (d) not blocked by TRPV1 receptor antagonism. Mechanisms underlying excitation of these afferent fibers in the early post-injury period will offer insights for development of novel pain relieving strategies in the early post-traumatic period. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4330275 Mon, 10 Jan 2011 00:00:00 +0100 4330275 http://www.medworm.com/index.php?rid=4330274&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F5 Previous studies in several different trigeminal nerve injury/inflammation models indicated that the hyperexcitability of primary afferent neurons contributes to the pain pathway underlying mechanical allodynia. Although multiple types of voltage-gated ion channels are associated with neuronal hyperexcitability, voltage-gated K+ channels (Kv) are one of the important physiological regulators of membrane potentials in excitable tissues, including nociceptive sensory neurons. Since the opening of K+ channels leads to hyperpolarization of cell membrane and a consequent decrease in cell excitability, several Kv channels have been proposed as potential target candidates for pain therapy. In this review, we focus on common changes measured in the Kv channels of several different trigeminal neuro... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4330274 Mon, 10 Jan 2011 00:00:00 +0100 4330274 http://www.medworm.com/index.php?rid=4322087&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F2 Conclusions: Ropivacaine provides prolonged analgesia possibly by suppressing microglial activation in an NGF-dependent manner and astrocyte activation in an NGF-independent manner in the dorsal spinal cord. Local anesthetics, including ropivacaine, may represent a new approach for glial cell inhibition and, therefore, therapeutic strategies for neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4322087 Fri, 07 Jan 2011 00:00:00 +0100 4322087 http://www.medworm.com/index.php?rid=4313515&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F7%2F1%2F1 Conclusions: These results suggest that prior exposure to a mild nerve lesion protects against adverse effects of subsequent neuropathic injury, and that this conditioning-induced inhibition of pain hypersensitivity is not dependent on neuroinflammation in DRGs and spinal cord. Identifying the underlying mechanisms may have important implications for the understanding of neuropathic pain due to nerve injury. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4313515 Wed, 05 Jan 2011 00:00:00 +0100 4313515 http://www.medworm.com/index.php?rid=4293111&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F98 Conclusions: QuAM is a suitable if not necessary tool to analyze activation of endogenous signalling in heterogeneous cultures. NGF, GDNF and EGF stimulation of DRG-neurons shows differential Erk1/2 activation responses and a corresponding differential behavioral phenotype. Thus, in addition to expression-markers also signalling-activity can be taken for functional subgroup differentiation and predictor of behavioral outcome. The anti-nociceptive function of EGF is an intriguing result in the context of tissue damage but also for understanding pain resulting from EGF-receptor block during cancer therapy. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4293111 Mon, 27 Dec 2010 00:00:00 +0100 4293111 http://www.medworm.com/index.php?rid=4274901&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F97 Conclusions: The analgesic potency of CTx FVIA and its greater reversibility could represent advantages over CTx-MVIIA for the treatment of refractory pain and contribute to the design of an analgesic with high potency and low side effects. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4274901 Tue, 21 Dec 2010 00:00:00 +0100 4274901 http://www.medworm.com/index.php?rid=4274902&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F96 Conclusions: Together, our data show that STOP null mice displayed elevated levels of endogenous morphine, as well as an increase of morphine receptor affinity and density in brain. This was correlated with hypernociception and impaired pharmacological sensitivity to mu opioid receptor ligands. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4274902 Mon, 20 Dec 2010 00:00:00 +0100 4274902 http://www.medworm.com/index.php?rid=4264326&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F95 Conclusions: Our results indicate that endogenous BDNF is involved in spinal sensitization following inflammation and that blockade of BDNF induction in DREAM transgenic mice underlies the failure to develop spinal sensitization. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4264326 Sat, 18 Dec 2010 00:00:00 +0100 4264326 http://www.medworm.com/index.php?rid=4264327&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F94 Conclusion: Behavioral recovery following peripheral RTX treatment is linked to regeneration of TRPV1-expressing Adelta and C-fibers and sustained expression of molecular markers. Infrared laser stimulation is a potentially valuable tool for evaluating the behavioral role of Adelta fibers in pain and pain control. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4264327 Fri, 17 Dec 2010 00:00:00 +0100 4264327 http://www.medworm.com/index.php?rid=4264328&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F93 In conclusion, mGluR1 rather than mGluR5 can account for the pain-related changes of excitatory and inhibitory synaptic transmission in the CeLC through a mechanism that involves inhibition of inhibitory transmission (disinhibition). (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4264328 Thu, 16 Dec 2010 00:00:00 +0100 4264328 http://www.medworm.com/index.php?rid=4248513&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F92 Conclusions: These results suggest that the selective ERalpha antagonist MPP pre-synaptically facilitates the excitatory synaptic transmission to SG neurons. The nociceptive transmission evoked by Adelta- and C-fiber stimulation could be potentiated by blocking ERalpha in the spinal neurons. Thus, the spinal estrogen may negatively regulate the nociceptive transmission through the activation of ERalpha. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4248513 Sat, 11 Dec 2010 00:00:00 +0100 4248513 http://www.medworm.com/index.php?rid=4248515&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F89 Conclusions: Our data indicate that specific glial cell populations become activated in both the trigeminal ganglia and the CNS following induction of temporomandibular joint inflammation, and suggest that they might represent innovative targets for controlling pain during trigeminal nerve sensitization. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4248515 Fri, 10 Dec 2010 00:00:00 +0100 4248515 http://www.medworm.com/index.php?rid=4248514&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F90 Conclusions: Overall, this study strengthens the important role of CCR2 in neuropathic pain and highlights feasibility that interfering on this mechanism at the spinal level with a selective antagonist can provide new analgesia opportunities. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4248514 Fri, 10 Dec 2010 00:00:00 +0100 4248514 http://www.medworm.com/index.php?rid=4241170&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F88 Conclusions: Nonproton ligand sensing domain might represent a novel mechanism for activation or sensitization of ASIC3 channels underlying inflammatory pain-sensing under in vivo conditions. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4241170 Wed, 08 Dec 2010 00:00:00 +0100 4241170 http://www.medworm.com/index.php?rid=4236861&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F87 Pain often accompanies cancer and most current therapies for treating cancer pain have significant unwanted side effects. Targeting nerve growth factor (NGF) or its cognate receptor tropomyosin receptor kinase A (TrkA) has become an attractive target for attenuating chronic pain.In the present report, we use a mouse model of bone cancer pain and examine whether oral administration of a selective small molecule Trk inhibitor (ARRY-470, which blocks TrkA, TrkB and TrkC kinase activity at low nm concentrations) has a significant effect on cancer-induced pain behaviors, tumor-induced remodeling of sensory nerve fibers, tumor growth and tumor-induced bone remodeling. Early/sustained (initiated day 6 post cancer cell injection), but not late/acute (initiated day 18 post cancer cell injection) ad... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4236861 Tue, 07 Dec 2010 00:00:00 +0100 4236861 http://www.medworm.com/index.php?rid=4232703&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F86 Conclusions: The opioid-neurotensin hybrid analogue PK20, in which opioid and neurotensin pharmacophores overlap partially, expresses high antinociceptive tail-flick effects after central as well as peripheral applications. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4232703 Mon, 06 Dec 2010 00:00:00 +0100 4232703 http://www.medworm.com/index.php?rid=4218950&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F85 Conclusion: LPA potentiates TRPV1 current via a PKCepsilon-dependent pathway in DRG neurons of rats with bone cancer, which may be a novel peripheral mechanism underlying the induction of bone cancer pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4218950 Wed, 01 Dec 2010 00:00:00 +0100 4218950 http://www.medworm.com/index.php?rid=4212882&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F84 Conclusions: NCX2, as well as NaV1.6, NaV1.7, NaV1.8 and NaV1.9, are present in most intra-epidermal free nerve endings. The presence of NCX2, together with multiple sodium channel isoforms, in free nerve endings may have important functional implications. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4212882 Tue, 30 Nov 2010 00:00:00 +0100 4212882 http://www.medworm.com/index.php?rid=4196282&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F82 This study examined the morphological and functional effects of oxaliplatin treatment in cultured adult rat DRG neurons. Results: 48 hour exposure to oxaliplatin resulted in dose related reduction in neurite length, density, and number of neurons compared to vehicle treated controls, using Gap43 immunostaining. Neurons treated acutely with 20 microg/ml oxaliplatin showed significantly higher signal intensity for cyclic AMP immunofluorescence (160.5 +/- 13 a.u., n=3, P (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4196282 Wed, 24 Nov 2010 00:00:00 +0100 4196282 http://www.medworm.com/index.php?rid=4175122&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F81 Conclusions: These findings show that two sets of forebrain structures mediate the initial sharp pain evoked by brief cutaneous heat stimulation: those responding preferentially to the brief stimulation of Adelta heat nociceptors and those with similar responses to converging inputs from the painless stimulation of C fibers. Our results suggest a unique and specific physiological basis, at the forebrain level, for the "first pain" sensation that has long been attributed to Adelta fiber stimulation and support the concept that both specific and convergent mechanisms act concurrently to mediate pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4175122 Wed, 17 Nov 2010 00:00:00 +0100 4175122 http://www.medworm.com/index.php?rid=4154757&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F79 Oro-facial pain following injury and infection is frequently observed in dental clinics. While neuropathic pain evoked by injury associated with nerve lesion has an involvement of glia/immune cells, inflammatory hyperalgesia has an exaggerated sensitization mediated by local and circulating immune mediators. To better understand the contribution of central nervous system (CNS) glial cells in these different pathological conditions, in this study we sought to characterize functional phenotypes of glial cells in response to trigeminal nerve injury (loose ligation of the mental branch), infection (subcutaneous injection of lipopolysaccharide-LPS) and to sterile inflammation (subcutaneous injection of complete Freund's adjuvant-CFA) on the lower lip. Each of the three insults triggered a speci... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4154757 Wed, 10 Nov 2010 00:00:00 +0100 4154757 http://www.medworm.com/index.php?rid=4149833&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F78 Conclusions: These results suggest that LPA, which is converted from LPC by ATX, activates LPA1 receptors and induces dorsal root demyelination following nerve injury, which causes neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4149833 Tue, 09 Nov 2010 00:00:00 +0100 4149833 http://www.medworm.com/index.php?rid=4149834&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F77 Conclusions: Presynaptic ephrin-B2 expression thus plays an important role in regulating inflammatory pain through the regulation of synaptic plasticity in the dorsal horn and is also involved in the pathogenesis of some types of neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4149834 Mon, 08 Nov 2010 00:00:00 +0100 4149834 http://www.medworm.com/index.php?rid=4138536&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F76 Conclusions: Minocycline prevents paclitaxel-evoked allodynia, likely due to its inhibition on loss of IENF, infiltration of macrophages and up-regulation of ATF3 in rats. The finding might provide potential target for preventing paclitaxel-induced neuropathic pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4138536 Fri, 05 Nov 2010 00:00:00 +0100 4138536 http://www.medworm.com/index.php?rid=4132532&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F75 Conclusions: Our results showed that the decreased extracellular levels of dopamine induced by inflammation correlated with the level of pain-related behaviour. These results also showed the increase in dopaminergic mediated inhibition by an increase in D2R's and a decrease in D1R's mRNA. There is a possible differential mechanism regarding the regulation of excitatory and inhibitory dopaminergic receptors triggered by inflammation. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4132532 Thu, 04 Nov 2010 00:00:00 +0100 4132532 http://www.medworm.com/index.php?rid=4132534&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F73 Conclusions: Our study has provided evidence supporting a view that acupuncture intervention involves complex modulations of temporal neural response, and its effect can gradually resolve as a function of time. The functional specificity of acupuncture at ST36 may involve multiple levels of differential activities of a wide range of brain networks, which are gradually enhanced even after acupuncture needle being terminated. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4132534 Tue, 02 Nov 2010 00:00:00 +0100 4132534 http://www.medworm.com/index.php?rid=4132533&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F74 Conclusions: We have discovered that injury to a peripheral nerve and electrical stimulation of C-fibers each cause an increase in the permeability of the BSCB and the BBB. The increase in permeability is delayed in onset, peaks at about 24 hours and is dependent upon action potential propagation. As the increase is mimicked by applying capsaicin to the nerve, the most parsimonious explanation for our findings is that the increase in permeability is mediated by activation of TRPV1-expressing primary sensory neurons. Our findings may be relevant to the development of pain and neuroplastic changes in the CNS following nerve injury. In addition, our findings may provide the basis for developing methods to purposefully open the BBB when needed to increase brain penetration of therapeutic agen... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4132533 Tue, 02 Nov 2010 00:00:00 +0100 4132533 http://www.medworm.com/index.php?rid=4117087&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F72 Conclusions: We have identified a novel pain cascade, in which IL-1beta production in cancer-inoculated regions induces ephrin B1 gene expression in DRGs and then ephrin B1 enhances the tyrosine phosphorylation of NR2B via Eph B receptor in the spinal cord. Notably, Z-360 relieves cancer-induced pain by preventing this pain cascade through the suppression of IL-1beta production, likely via the blockade of CCK1 receptor. The pre-clinical results presented here support the analgesic action of Z-360 in pancreatic cancer patients with severe, opioid-resistant pain. Pre-clinical and clinical results have demonstrated that Z-360 combined with gemcitabine represents a promising pancreatic cancer therapy approach with characteristic analgesic effects in addition to the prolongation of survival. (S... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4117087 Wed, 27 Oct 2010 23:00:00 +0100 4117087 http://www.medworm.com/index.php?rid=4117089&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F70 Conclusion: The results suggest that chronic nerve injury evoked hypernociception may be contributed by genetic differences of descending serotonergic inhibitory control. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4117089 Mon, 25 Oct 2010 23:00:00 +0100 4117089 http://www.medworm.com/index.php?rid=4117088&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F71 Conclusions: These findings demonstrate that delta-opioid receptor activation selectively inhibits inputs activated by icilin, whereas mu-opioid receptor activation has a more widespread effect on synaptic inputs to neurons in the superficial dorsal horn. These findings suggest that delta-opioids may provide a novel analgesic approach for specific, TRPA1-like mediated pain modalities. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4117088 Mon, 25 Oct 2010 23:00:00 +0100 4117088 http://www.medworm.com/index.php?rid=4104811&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F69 Conclusions: It appears that morphine administration can induce long-lasting genomic effects in different body areas which contribute to the strong central and peripheral testosterone levels. These changes were not always accompanied by behavioral modifications. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4104811 Mon, 25 Oct 2010 23:00:00 +0100 4104811 http://www.medworm.com/index.php?rid=4104812&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F68 The pathophysiology of migraine remains largely unknown. However, evidence regarding the molecules participating in the pathophysiology of migraine has been accumulating. Water channel proteins, known as aquaporins (AQPs), notably AQP-1 and AQP-4, appears to be involved in the pathophysiology of several neurological diseases. This review outlines newly emerging evidence indicating that AQP-1 plays an important role in pain signal transduction and migraine and could therefore serve as a potential therapeutic target for these diseases. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4104812 Sun, 24 Oct 2010 23:00:00 +0100 4104812 http://www.medworm.com/index.php?rid=4096023&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F67 The neuropeptide galanin is widely expressed in both the central and peripheral nervous systems and is involved in many diverse biological functions. There is a substantial data set that demonstrates galanin is upregulated after injury in the DRG, spinal cord and in many brain regions where it plays a predominantly antinociceptive role in addition to being neuroprotective and pro-regenerative. To further characterise the role of galanin following nerve injury, a novel transgenic line was created using the binary transgenic tet-off system, to overexpress galanin in galaninergic tissue in a suppressible manner. The double transgenic mice express significantly more galanin in the DRG one week after sciatic nerve section (axotomy) compared to WT mice and this overexpression is suppressible upo... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4096023 Wed, 20 Oct 2010 23:00:00 +0100 4096023 http://www.medworm.com/index.php?rid=4055338&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F66 Transient receptor potential vanilloid type 1(TRPV1)receptor is a non selective ligand-gated cation channel activated by capsaicin, heat, protons and endogenous lipids termed endovanilloids. As well as peripheral primary afferent neurons and dorsal root ganglia, TRPV1 receptor is also expressed in spinal and supraspinal structures such as those belonging to the endogenous antinociceptive descending pathway which is a circuitry of the supraspinal central nervous system whose task is to counteract pain. It includes periaqueductal grey (PAG) and rostral ventromedial medulla (RVM) whose activation leads to analgesia. Such an effect is associated with a glutamate increase and the activation of OFF and inhibition of ON cell population in the rostral ventromedial medulla (RVM). Activation of the ... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4055338 Sun, 10 Oct 2010 23:00:00 +0100 4055338 http://www.medworm.com/index.php?rid=4035776&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F65 Conclusions: We found that an inducible expression of Kir2.1 channels in chronically compressed DRG neurons can effectively suppress the neuronal excitability and, if induced at the beginning of CCD injury, prevent the development of hyperalgesia. We hypothesize that a higher level of neuronal hyperexcitability in the DRG is required to initiate than to maintain the hyperalgesia and that the hyperexcitability contributing to neuropathic pain is best inhibited as soon as possible after injury. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4035776 Tue, 05 Oct 2010 23:00:00 +0100 4035776 http://www.medworm.com/index.php?rid=4035777&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F64 Conclusions: These results suggest that thalidomide can efficiently alleviate bone cancer pain and it may be a useful alternative or adjunct therapy for bone cancer pain. Our data also suggest a role of spinal TNF-alpha in the development of bone cancer pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4035777 Mon, 04 Oct 2010 23:00:00 +0100 4035777 http://www.medworm.com/index.php?rid=4030358&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F63 Conclusion: These results suggest that caspase-1 plays a critical role in the cascade of events involved in the genesis of inflammatory hypernociception by promoting IL-1b maturation. Because caspase-1 is involved in the induction of COX-2 expression and PGE2 production, our data support the assertion that caspase-1 is a key target to control inflammatory pain. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4030358 Sun, 03 Oct 2010 23:00:00 +0100 4030358 http://www.medworm.com/index.php?rid=4011564&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F62 The anterior cingulate cortex (ACC) plays important roles in emotion, learning, memory and persistent pain. Our previous in vitro studies have demonstrated that pyramidal neurons in layer II/III of the adult mouse ACC can be characterized into three types: regular spiking (RS), intermediate (IM) and intrinsic bursting (IB) cells, according to their action potential (AP) firing patterns. However, no in vivo information is available for the intrinsic properties and sensory responses of ACC neurons of adult mice. Here, we performed in vivo whole-cell patch-clamp recordings from pyramidal neurons in adult mice ACC under urethane anesthetized conditions. First, we classified the intrinsic properties and analyzed their slow oscillations. The population ratios of RS, IM and IB cells were 10, 62 a... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4011564 Mon, 27 Sep 2010 23:00:00 +0100 4011564 http://www.medworm.com/index.php?rid=4011565&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F61 Protease-activated receptors (PAR1-4) are activated by proteases released by cell damage or blood clotting, and are known to be involved in promoting pain and hyperalgesia. Previous studies have shown that PAR2 receptors enhance activation of TRPV1 but the role of other PARs is less clear. In this paper we investigate the expression and function of the PAR1, 3 and 4 thrombin-activated receptors in sensory neurones. Immunocytochemistry and in situ hybridization show that PAR1 and PAR4 are expressed in 10 - 15% of neurons, distributed across all size classes. Thrombin or a specific PAR1 or PAR4 activating peptide (PAR1/4-AP) caused functional effects characteristic of activation of the PLC/PKC pathway: intracellular calcium release, sensitisation of TRPV1, and translocation of the epsilon is... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=4011565 Sun, 26 Sep 2010 23:00:00 +0100 4011565 http://www.medworm.com/index.php?rid=3992650&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F59 Background, To evaluate whether P2X receptors are involved in responses to noxious pulp stimulation, the P2X3 and P2X2/3 receptor agonist alpha,beta-methyleneATP (alpha,beta-meATP) was applied to the molar tooth pulp and nocifensive behavior and extracellular-signal regulated kinase (ERK) phosphorylation in trigeminal spinal subnucleus caudalis (Vc), trigeminal spinal subnucleus interpolaris (Vi), upper cervical spinal cord (C1/C2) and paratrigeminal nucleus (Pa5) neurons were analyzed in rats.Results, Genioglossus (GG) muscle activity was evoked by pulpal application of 100 mM alpha,beta-meATP and was significantly larger than GG activity following vehicle (phosphate-buffered saline PBS) application (p (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3992650 Tue, 21 Sep 2010 23:00:00 +0100 3992650 http://www.medworm.com/index.php?rid=3992649&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F60 Conclusions: The main finding of this study is that NAAG and NAAG peptidase inhibition reduce excitatory neurotransmission and inflammation-induced plasticity at the spinoparabrachial synapse within the pain processing pathway of the central amygdaloid nucleus. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3992649 Tue, 21 Sep 2010 23:00:00 +0100 3992649 http://www.medworm.com/index.php?rid=3992651&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F58 Conclusions: Results obtained here suggest that increased heat sensitivity in TRPV1-negative CPM-fibers alone following inflammation is insufficient for the induction of heat hyperalgesia. On the other hand, TRPV1-positive CH fibers appear to play an essential role in this process that may include both afferent and efferent functions. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3992651 Mon, 20 Sep 2010 23:00:00 +0100 3992651 http://www.medworm.com/index.php?rid=3976059&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F56 Conclusion: Evaluation of phenoxybenzamine-induced analgesia in the current study lends support to the utility of the Connectivity Map approach for identifying compounds with analgesic properties in the CFA model. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3976059 Wed, 15 Sep 2010 23:00:00 +0100 3976059 http://www.medworm.com/index.php?rid=3972404&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F55 Conclusion: We suggest that at this early stage of inflammatory pain in man, NO is analgesic in the periphery. Further, ketorolac down-regulates eNOS gene expression. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3972404 Tue, 14 Sep 2010 23:00:00 +0100 3972404 http://www.medworm.com/index.php?rid=3968570&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F54 Descending controls originating in part from the rostral ventromedial medulla (RVM) regulate the excitability of dorsal horn neurons and maintain peripheral pain states. Activation of extracellular signal regulated kinase (ERK) in RVM neurons has been shown following peripheral inflammation and is involved in generating the accompanying inflammatory hyperalgesia. Here, we show that spared nerve injury (SNI), a model of neuropathic pain, results in an increase in ERK activity in RVM neurons of adult rats 3 and 8 days following surgery. We carried out two experimental procedures to demonstrate that this increase in ERK activation was related to the increased mechanical sensitivity associated with SNI. First, we showed that lesions of the lamina I/III ascending pathway from the dorsal horn at... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3968570 Mon, 13 Sep 2010 23:00:00 +0100 3968570 http://www.medworm.com/index.php?rid=3964960&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F52 Gastrin-releasing peptide (GRP) has been proposed as a peptidergic molecule for behavioral fear and itching. Immunohistochemistry and in situ hybridization studies have shown that GRP and GRP receptor are widely distributed in forebrain areas. Less information is available for the functional action for GRP in the prefrontal cortex including the anterior cingulate cortex (ACC). Here we used whole-cell patch-clamp recording technique to study the modulation of synaptic transmission by GRP in the ACC. We found that GRP increased the frequency of sIPSCs recorded while had no significant effect on sEPSCs in ACC pyramidal neurons. The facilitatory effect of GRP on sIPSCs was blocked by the GRP receptor antagonist, RC3095. In the presence of TTX, however, GRP had no effect on the mIPSCs. Therefor... Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3964960 Sun, 12 Sep 2010 23:00:00 +0100 3964960 http://www.medworm.com/index.php?rid=3964959&cid=s_34084_67_f&fid=34084&url=http%3A%2F%2Fwww.molecularpain.com%2Fcontent%2F6%2F1%2F53 Conclusions: In conclusion, adult rat DRG tissue exhibits a specific pattern of expression of copper transporters with distinct subsets of peripheral sensory neurons intensely expressing either ATP7A or CTR1, but not both or ATP7B. The neuron subtype-specific and largely non-overlapping distribution of ATP7A and CTR1 within rat DRG tissue may be required to support the differing cuproenzyme requirements of distinct subsets of sensory neurons, and could influence the transport and neurotoxicity of oxaliplatin. (Source: Molecular Pain) Molecular Pain journals http://www.medworm.com/rss/comments.php?id=3964959 Sun, 12 Sep 2010 23:00:00 +0100 3964959