Analgesia for neuropathic pain by dorsal root ganglion transplantation of genetically engineered mesenchymal stem cells: initial results
Conclusions:
These data indicate that genetically modified MSCs secreting analgesic peptides could potentially be developed as a novel DRG-targeted cell therapy for treating neuropathic pain. However, further work is needed to address the challenges of MSC survival and excess proliferation, possibly with trials of autologous MSCs, evaluation of clonally selected populations of MSCs, and investigation of regulation of MSC proliferation. (Source: Molecular Pain)
Source: Molecular Pain - February 12, 2015 Category: Molecular Biology Authors: Hongwei YuGregory FischerAllison EbertHsiang-En WuXiaowen BaiQuinn Hogan Source Type: research
Attenuation of inflammatory and neuropathic pain behaviors in mice through activation of free fatty acid receptor GPR40
Conclusions:
Our results indicate that GPR40 signaling pathway plays an important suppressive role in spinal nociceptive processing after inflammation or nerve injury, and that GPR40 agonists might serve as a new class of analgesics for treating inflammatory and neuropathic pain. (Source: Molecular Pain)
Source: Molecular Pain - February 12, 2015 Category: Molecular Biology Authors: Prasanna KarkiTakashi KuriharaTomoya NakamachiJun WatanabeToshihide AsadaTatsuki OyoshiSeiji ShiodaMegumu YoshimuraKazunori AritaAtsuro Miyata Source Type: research
Spinal autophagy is differently modulated in distinct mouse models of neuropathic pain
In this study, we characterized the main autophagic markers in two other common experimental models of neuropathic pain, the chronic constriction injury (CCI) and the spared nerve injury (SNI). The different modulation of LC3-I, Beclin 1 and p62 suggested that autophagy is differentially affected in the spinal dorsal horn depending on the type of peripheral injury. Confocal analysis of p62 distribution in the spinal dorsal horn indicated its presence mainly in NeuN-positive cell bodies and occasionally in glial processes, thus suggesting a predominant expression in the neuronal compartment. Finally, we investigated the con...
Source: Molecular Pain - February 2, 2015 Category: Molecular Biology Authors: Laura BerliocchiMaria MaiarùGiuseppe VaranoRossella RussoMaria CorasanitiGiacinto BagettaCristina Tassorelli Source Type: research
Protein kinase C¿ mediates histamine-evoked itch and responses in pruriceptors
Conclusions:
Our findings indicate that PKCdelta plays a role in mediating histamine-induced itch, but may be dispensable for chloroquine- and beta-alanine-induced itch. (Source: Molecular Pain)
Source: Molecular Pain - January 6, 2015 Category: Molecular Biology Authors: Manouela ValtchevaSteve DavidsonChengshui ZhaoMichael LeitgesRobert Gereau Source Type: research
Variability in C-type lectin receptors regulates neuropathic pain-like behavior after peripheral nerve injury
Conclusion:
We here for the first time demonstrate that C-type lectins, a family of innate immune receptors with largely unknown functions in the nervous system, are involved in regulation of inflammation and development of neuropathic pain behavior after nerve injury. Further experimental and clinical studies are needed to dissect the underlying mechanisms more in detail as well as any possible relevance for human conditions. (Source: Molecular Pain)
Source: Molecular Pain - December 10, 2014 Category: Molecular Biology Authors: Cecilia DominguezKarl CarlströmXing-Mei ZhangFaiez Al NimerRickard LindblomAndre Ortlieb Guerreiro-CacaisFredrik Piehl Source Type: research
NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors
Conclusions:
Overall, our work shows that NMP-7 mediates a significant analgesic effect in a model of persistent inflammatory and chronic neuropathic pain by way of T-type channel modulation and CB2 receptor activation. Thus, this study provides a novel therapeutic avenue for managing chronic pain conditions via mixed CB ligands/T-type channel blockers. (Source: Molecular Pain)
Source: Molecular Pain - December 6, 2014 Category: Molecular Biology Authors: N BergerVinicius GadottiRavil PetrovKevin ChapmanPhilippe DiazGerald Zamponi Source Type: research
NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors
Conclusions:
Overall, our work shows that NMP-7 mediates a significant analgesic effect in a model of persistent inflammatory and chronic neuropathic pain by way of T-type channel modulation and CB2 receptor activation. Thus, this study provides a novel therapeutic avenue for managing chronic pain conditions via mixed CB ligands/T-type channel blockers. (Source: Molecular Pain)
Source: Molecular Pain - December 6, 2014 Category: Molecular Biology Authors: Nelson BergerVinicius GadottiRavil PetrovKevin ChapmanPhilippe DiazGerald Zamponi Source Type: research
No association of polymorphisms in the serotonin transporter gene with thermal pain sensation in healthy individuals
Conclusions:
Genotypes associated with high or low expression of the serotonin transporter were not associated with thermal pain thresholds, pressure pain threshold, pain after capsaicin application or responses to the thermal grill.The present results do not support that the investigated genotypes play a major role in thermal pain perception among healthy individuals. (Source: Molecular Pain)
Source: Molecular Pain - December 4, 2014 Category: Molecular Biology Authors: Ellen SchaldemoseEmilia Horjales-AraujoDitte DemontisAnders BørglumPeter SvenssonNanna Finnerup Source Type: research
Haplotypes of P2RX7 gene polymorphisms are associated with both cold pain sensitivity and analgesic effect of fentanyl
Conclusions:
Cold pain sensitivity and analgesic effects of fentanyl were related to the SNP and haplotypes of the P2RX7 gene. The patients with the rs1718125 G>A SNP tended to show higher VAS24 scores. Moreover, the combination of polymorphisms from the 5[prime]-flanking region to exon 5 recessively affected cold pain sensitivity and analgesic effects of opioids for acute cold pain. The present findings shed light on the involvement of P2RX7 gene polymorphisms in naive cold pain sensitivity and analgesic effects of fentanyl. (Source: Molecular Pain)
Source: Molecular Pain - December 3, 2014 Category: Molecular Biology Authors: Soichiro IdeDaisuke NishizawaKen-ichi FukudaShinya KasaiJunko HasegawaMasakazu HayashidaMasabumi MinamiKazutaka Ikeda Source Type: research
Sphingosine 1-phosphate to p38 signaling via S1P1 receptor and G¿i/o evokes augmentation of capsaicin-induced ionic currents in mouse sensory neurons
In this study, the S1P mediated signaling pathway required for sensitization of TRPV1 channels was explored.The capsaicin induced peak inward current (ICAPS) of sensory neurons was significantly increased after S1P stimulation within minutes after application. The potentiation of ICAPS resulted from activation of Galphai through G-protein coupled receptors for S1P. Consequently, Galphai led to a signaling cascade, involving phosphoinositide-3-kinase (PI3K) and protein kinase C, which augmented ICAPS in nociceptive neurons. The S1P1 receptor agonist SEW2871 resulted in activation of the same signaling pathway and potentiati...
Source: Molecular Pain - November 28, 2014 Category: Molecular Biology Authors: Michiel LangeslagSerena QuartaMichael LeitnerMichaela KressNorbert Mair Source Type: research
Sphingosine 1-phosphate to p38 signaling via S1P1 receptor and Galphai/o evokes augmentation of capsaicin-induced ionic currents in mouse sensory neurons
In this study, the S1P mediated signaling pathway required for sensitization of TRPV1 channels was explored.The capsaicin induced peak inward current (ICAPS) of sensory neurons was significantly increased after S1P stimulation within minutes after application. The potentiation of ICAPS resulted from activation of Galphai through G-protein coupled receptors for S1P. Consequently, Galphai led to a signaling cascade, involving phosphoinositide-3-kinase (PI3K) and protein kinase C, which augmented ICAPS in nociceptive neurons. The S1P1 receptor agonist SEW2871 resulted in activation of the same signaling pathway and potentiati...
Source: Molecular Pain - November 28, 2014 Category: Molecular Biology Authors: Michiel LangeslagSerena QuartaMichael LeitnerMichaela KressNorbert Mair Source Type: research
Enhanced behavioral responses to cold stimuli following CGRP¿ sensory neuron ablation are dependent on TRPM8
Conclusions:
Our data indicate that the enhanced behavioral responses to cold stimuli in CGRPalpha sensory neuron-ablated mice are dependent on functional TRPM8, whereas the other sensory and thermoregulatory phenotypes caused by CGRPalpha sensory neuron ablation are independent of TRPM8. (Source: Molecular Pain)
Source: Molecular Pain - November 19, 2014 Category: Molecular Biology Authors: Eric McCoyMark Zylka Source Type: research
Enhanced behavioral responses to cold stimuli following CGRPalpha sensory neuron ablation are dependent on TRPM8
Conclusions:
Our data indicate that the enhanced behavioral responses to cold stimuli in CGRPalpha sensory neuron-ablated mice are dependent on functional TRPM8, whereas the other sensory and thermoregulatory phenotypes caused by CGRPalpha sensory neuron ablation are independent of TRPM8. (Source: Molecular Pain)
Source: Molecular Pain - November 19, 2014 Category: Molecular Biology Authors: Eric McCoyMark Zylka Source Type: research
Optogenetic activation of brainstem serotonergic neurons induces persistent pain sensitization
Conclusions:
These results suggest that selective activation of RVM 5-HT neurons exerts a predominant effect of pain facilitation under control conditions. (Source: Molecular Pain)
Source: Molecular Pain - November 19, 2014 Category: Molecular Biology Authors: You-Qing CaiWei WangYuan-Yuan HouZhizhong Pan Source Type: research
Lysophosphatidic acid and its receptors LPA1 and LPA3 mediate paclitaxel-induced neuropathic pain in mice
Conclusions:
These results suggest that LPA1 and LPA3 receptors-mediated amplification of spinal LPA production is required for the development of paclitaxel-induced neuropathic pain. (Source: Molecular Pain)
Source: Molecular Pain - November 19, 2014 Category: Molecular Biology Authors: Hitoshi UchidaJun NagaiHiroshi Ueda Source Type: research
