Reviewer acknowledgement
Contributing reviewersThe editors of Molecular Pain would like to thank all the reviewers who have contributed to the journal in Volume 8 (2012). (Source: Molecular Pain)
Source: Molecular Pain - March 22, 2013 Category: Molecular Biology Authors: Jianguo GuMin Zhuo Source Type: research
BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state
Conclusions:
Hence, BDNF is a key regulator of aPKC synthesis and phosphorylation and an essential mediator of the maintenance of a centralized chronic pain state. These findings point to BDNF regulation of aPKC as a potential therapeutic target for the permanent reversal of a chronic pain state. (Source: Molecular Pain)
Source: Molecular Pain - March 20, 2013 Category: Molecular Biology Authors: Ohannes MelemedjianDipti TilluMarina AsieduEdward MandellJamie MoyVictoria BluteCaleb TaylorSourav GhoshTheodore Price Source Type: research
Involvement of TRPA1 activation in acute pain induced by cadmium in mice
Conclusions:
Cd excites sensory neurons via activation of TRPA1 and causes acute pain, the mechanism of which may be similar to that of Zn. The present results indicate that TRPA1 is involved in the nociceptive or inflammatory effects of Cd. (Source: Molecular Pain)
Source: Molecular Pain - February 28, 2013 Category: Molecular Biology Authors: Saeko MiuraKenji TakahashiToshiaki ImagawaKunitoshi UchidaShigeru SaitoMakoto TominagaToshio Ohta Source Type: research
ZIPping to pain relief: the role (or not) of PKMzeta in chronic pain
Chronic pain remains a significant clinical problem despite substantial advances in our understanding of how persistent nociceptor stimulation drives plasticity in the CNS. A major theme that has emerged in this area of work is the strong similarity between plasticity involved in learning and memory in CNS regions such as cortex and hippocampus with mechanisms underlying chronic pain development and maintenance in the spinal dorsal horn and other CNS areas such as anterior cingulate cortex (ACC). We, and others have recently implicated an atypical PKC (aPKC), called PKMzeta, in the maintenance of pain plasticity based on b...
Source: Molecular Pain - February 22, 2013 Category: Molecular Biology Authors: Theodore PriceSourav Ghosh Source Type: research
Impaired behavioural pain responses in hph-1 mice with inherited deficiency in GTP cyclohydrolase 1 in models of inflammatory pain
Conclusions:
In this study, we demonstrate novel evidence that genetic mutations in the GCH1 gene modulate pain-like hypersensitivity. Together, the present data suggest that BH4 is not important for basal heat and mechanical pain, but they support the hypothesis that BH4 plays a role in inflammation-induced hypersensitivity. Our studies suggest that the BH4 pathway could be a therapeutic target for the treatment of inflammatory pain conditions. Moreover, the hph-1 mice provide a valid model to study the consequence of congenital deficiency of GCH1 in painful conditions. (Source: Molecular Pain)
Source: Molecular Pain - February 19, 2013 Category: Molecular Biology Authors: Arafat NasserOle BjerrumAnne-Marie HeegaardAnette MøllerMajbritt LarsenLouise DalbøgeErik DupontTroels JensenLisbeth Møller Source Type: research
Hydrogen sulfide increases excitability through suppression of sustained potassium channel currents of rat trigeminal ganglion neurons
Conclusion:
These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. (Source: Molecular Pain)
Source: Molecular Pain - February 18, 2013 Category: Molecular Biology Authors: Xingmei FengYou-Lang ZhouXiaowen MengFei-Hu QiWei ChenXinghong JiangGuang-Yin Xu Source Type: research
Modulation of TRP channels by resveratrol and other stilbenoids
Conclusions:
These data suggest that resveratrol and other stilbenoids may have an inhibitory effect on TRP channels. In addition, these stilbenoids modulate TRP channel activity in different ways. (Source: Molecular Pain)
Source: Molecular Pain - February 15, 2013 Category: Molecular Biology Authors: Lina YuShenglan WangYoko KogureSatoshi YamamotoKoichi NoguchiYi Dai Source Type: research
Effect of cholesterol depletion on the pore dilation of TRPV1
The TRPV1 ion channel is expressed in nociceptors, where pharmacological modulation of its function may offer a means of alleviating pain and neurogenic inflammation processes in the human body. The aim of this study was to investigate the effects of cholesterol depletion of the cell on ion-permeability of the TRPV1 ion channel. The ion-permeability properties of TRPV1 were assessed using whole-cell patch-clamp and YO-PRO uptake rate studies on a Chinese hamster ovary (CHO) cell line expressing this ion channel. Prolonged capsaicin-induced activation of TRPV1 with N-methyl-D-glucamine (NMDG) as the sole extracellular catio...
Source: Molecular Pain - January 2, 2013 Category: Molecular Biology Authors: Erik JanssonCarolina TrkuljaAikeremu AhemaitiMaria MillingenGavin JeffriesKent JardemarkOwe Orwar Source Type: research
Effect of cholesterol depletion on the pore dilation of TRPV1
The TRPV1 ion channel is expressed in nociceptors, where pharmacological modulation of its function may offer a means of alleviating pain and neurogenic inflammation processes in the human body. The aim of this study was to investigate the effects of cholesterol depletion of the cell on ion-permeability of the TRPV1 ion channel. The ion-permeability properties of TRPV1 were assessed using whole-cell patch-clamp and YO-PRO uptake rate studies on a Chinese hamster ovary (CHO) cell line expressing this ion channel. Prolonged capsaicin-induced activation of TRPV1 with N-methyl-D-glucamine (NMDG) as the sole extracellular catio...
Source: Molecular Pain - January 2, 2013 Category: Molecular Biology Authors: Erik JanssonCarolina TrkuljaAikeremu AhemaitiMaria MillingenGavin JeffriesKent JardemarkOwe Orwar Source Type: research
Genetic enhancement of neuropathic and inflammatory pain by forebrain upregulation of CREB-mediated transcription
CREB has been reported to be activated by injury and is commonly used as marker for pain-related plasticity changes in somatosensory pathways, including spinal dorsal horn neurons and the anterior cingulate cortex (ACC). However no evidence has been reported to support the direct role of activated CREB in injury-related behavioral sensitization (or allodynia). Here we report that genetic enhancement of CREB-mediated transcription selectively in forebrain areas enhanced behavioral responses to non-noxious stimuli after chronic inflammation (CFA model) or nerve injury. In contrast, behavioral acute responses to peripheral su...
Source: Molecular Pain - December 31, 2012 Category: Molecular Biology Authors: Giannina DescalziHotaka FukushimaAkinobu SuzukiSatoshi KidaMin Zhuo Source Type: research
