Transient receptor potential ankyrin 1 that is induced in dorsal root ganglion neurons contributes to acute cold hypersensitivity after oxaliplatin administration
Conclusions:
Together, these results demonstrate that TRPA1 expression via activation of p38 MAPK in DRG neurons, at least in part, contributes to the development of oxaliplatin-induced acute cold hyperalgesia. (Source: Molecular Pain)
Source: Molecular Pain - November 13, 2015 Category: Molecular Biology Authors: Ken YamamotoNoriko ChibaTerumasa ChibaToshie KambeKenji AbeKazuyoshi KawakamiIku UtsunomiyaKyoji Taguchi Source Type: research
p38 MAPK mediates glial P2X7R-neuronal P2Y1R inhibitory control of P2X3R expression in dorsal root ganglion neurons
Conclusions:
p38 in DRG neurons downstream of P2Y1R is necessary and sufficient for the P2X7R-P2Y1R inhibitory control of P2X3R expression. (Source: Molecular Pain)
Source: Molecular Pain - November 5, 2015 Category: Molecular Biology Authors: Yong ChenGuangwen LiLi-Yen Huang Source Type: research
The modulation effect of longitudinal acupuncture on resting state functional connectivity in knee osteoarthritis patients
In this study, we investigated functional connectivity across longitudinal acupuncture treatments in older patients with knee osteoarthritis (OA). Over a period of 4 weeks (six treatments), we collected resting state functional magnetic resonance imaging (fMRI) scans from 30 patients before and after their first, third and sixth treatments. Clinical outcome showed a significantly greater pain subscore on the Knee Injury and Osteoarthritis Outcome Score (KOOS) (indicative of improvement) with verum acupuncture than with sham acupuncture. Independent component analysis (ICA) of the resting state fMRI data showed that the ri...
Source: Molecular Pain - October 29, 2015 Category: Molecular Biology Authors: Xiaoyan ChenRosa SpaethSonya FreemanDonna ScarboroughJaveria HashmiHsiao-Ying WeyNatalia EgorovaMark VangelJianren MaoAjay WasanRobert EdwardsRandy GollubJian Kong Source Type: research
Contribution of Piezo2 to endothelium-dependent pain
Conclusions:
These results support the hypothesis that Piezo2 is a mechano-transducer in the endothelial cell where it contributes to stimulus-dependent hyperalgesia, and a model of chemotherapy-induced painful peripheral neuropathy. (Source: Molecular Pain)
Source: Molecular Pain - October 24, 2015 Category: Molecular Biology Authors: Luiz FerrariOliver BogenPaul GreenJon Levine Source Type: research
MicroRNA circulating in the early aftermath of motor vehicle collision predict persistent pain development and suggest a role for microRNA in sex-specific pain differences
Background:
Molecular mediators influencing the transition from acute to persistent musculoskeletal pain following common stress exposures such as motor vehicle collision (MVC) remain poorly understood. In this exploratory, proof of concept study, we compared circulating microRNA (miRNA) expression profiles in the early aftermath of MVC among individuals who did and did not subsequently develop persistent pain. Blood RNA samples were obtained from African American individuals (n = 53) who presented to the emergency department after MVC and were discharged to home after evaluation. The presence or absence of severe pain i...
Source: Molecular Pain - October 24, 2015 Category: Molecular Biology Authors: Sarah LinnstaedtMargaret WalkerJoel ParkerEunice YehRobert SonsErin ZimnyChristopher LewandowskiPhyllis HendryKathia DamironClaire PearsonMarc-Anthony VelillaBrian O¿NeilJeffrey JonesRobert SworRobert DomeierScott HammondSamuel McLean Source Type: research
Transient, activity dependent inhibition of transmitter release from low threshold afferents mediated by GABA A receptors in spinal cord lamina III/IV
Conclusions:
These observations suggest that afferent driven release of GABA onto low threshold afferent terminals is most effective following the first action potential in a train and serves to suppress the initial strong excitatory drive onto dorsal horn circuitry. (Source: Molecular Pain)
Source: Molecular Pain - October 13, 2015 Category: Molecular Biology Authors: Chiara BetelliAmy MacDermottRita Bardoni Source Type: research
Novel cytogenic and neurovascular niches due to blood–brain barrier compromise in the chronic pain brain
Background:
The mechanisms by which painful injuries are linked to the multitude of pain-related comorbidities and neuroplastic changes in the brain remain poorly understood. Here we propose a model that relies on epi-neuronal communication through the vascular system to effect various brain structures. Specifically, we hypothesize that the differential vulnerability of the blood–brain barrier (BBB) in different brain regions is associated with region-specific neuroplastic and neurovascular changes that are in turn associated with particular pain-related comorbidities.Presentation of the hypothesisWe will present our hyp...
Source: Molecular Pain - October 9, 2015 Category: Molecular Biology Authors: Maral TajerianJ. Clark Source Type: research
Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons
Conclusion:
INaRs are associated with inherited and acquired pain disorders. However, our ability to selectively target and study this current has been hindered due to limited understanding of how it is generated in sensory neurons. This study identified Navβ4 as an important regulator of INaR and excitability in sensory neurons. As such, Navβ4 is a potential target for the manipulation of pain sensations. (Source: Molecular Pain)
Source: Molecular Pain - September 25, 2015 Category: Molecular Biology Authors: Cindy BarbosaZhi-Yong TanRuizhong WangWenrui XieJudith StrongReesha PatelMichael VaskoJun-Ming ZhangTheodore Cummins Source Type: research
Pirt contributes to uterine contraction-induced pain in mice
Uterine contraction-induced pain (UCP) represents a common and severe form of visceral pain. Nerve fibers that innervate uterine tissue express the transient receptor potential vanilloid channel 1 (TRPV1), which has been shown to be involved in the perception of UCP. The phosphoinositide-interacting regulator of TRP (Pirt) may act as a regulatory subunit of TRPV1. The intraperitoneal injection of oxytocin into female mice after a 6-day priming treatment with estradiol benzoate induces writhing responses, which reflect the presence of UCP. Here, we first compared writhing response between Pirt
...
Source: Molecular Pain - September 17, 2015 Category: Molecular Biology Authors: Changming WangZhongli WangYan YangChan ZhuGuanyi WuGuang YuTunyu JianNiuniu YangHao ShiMin TangQian HeLei LanQin LiuYun GuanXinzhong DongJinao DuanZongxiang Tang Source Type: research
Mitochondrial and bioenergetic dysfunction in trauma-induced painful peripheral neuropathy
Conclusion:
Traumatic peripheral nerve injury induces persistent mitochondrial and bioenergetic dysfunction which implies that pharmacological agents which seek to normalize mitochondrial and bioenergetic dysfunction could be expected to be beneficial for pain treatment. Increases in both glycolytic acidification and non-glycolytic acidification suggest that pH sensitive drugs which preferentially act on acidic tissue will have the ability to preferential act on injured nerves without affecting healthy tissues. (Source: Molecular Pain)
Source: Molecular Pain - September 17, 2015 Category: Molecular Biology Authors: Tony LimMalena RoneSeunghwan LeeJack AntelJi Zhang Source Type: research
Sympathetic fibre sprouting in the skin contributes to pain-related behaviour in spared nerve injury and cuff models of neuropathic pain
Conclusions:
Alterations in sympathetic innervation in the skin represents an important mechanism that contributes to pain in cuff and SNI models of neuropathic pain. (Source: Molecular Pain)
Source: Molecular Pain - September 17, 2015 Category: Molecular Biology Authors: Francisney NascimentoClaire MagnussenNoosha YousefpourAlfredo Ribeiro-da-Silva Source Type: research
Anoctamin-1 Cl − channels in nociception: activation by an N-aroylaminothiazole and capsaicin and inhibition by T16A[inh]-A01
Conclusions:
An ANO1-activator (E-act) induced [Cl
−
]
i
-dependent sensory neuronal action potentials and mouse nocifensive behaviors; thus, direct ANO1 activation can induce pain perception. ANO1-inhibition attenuated capsaicin-triggering of action potentials and capsaicin-induced nocifensive behaviors. These results indicate ANO1 channels are involved with TRPV1 actions in sensory neurons and inhibition of ANO1 could be a novel means of inducing analgesia. (Source: Molecular Pain)
Source: Molecular Pain - September 12, 2015 Category: Molecular Biology Authors: Farah DebaBret Bessac Source Type: research
Alleviating neuropathic pain mechanical allodynia by increasing Cdh1 in the anterior cingulate cortex
Conclusions:
These results provide evidence that Cdh1 in ACC synapses may offer a novel therapeutic strategy for treating chronic neuropathic pain. (Source: Molecular Pain)
Source: Molecular Pain - September 12, 2015 Category: Molecular Biology Authors: Wei TanWen-Long YaoRong HuYou-You LvLi WanChuan-Han ZhangChang Zhu Source Type: research
Limited changes in spinal lamina I dorsal horn neurons following the cytotoxic ablation of non-peptidergic C-fibers
Conclusions:
Our results demonstrate that the deletion of the non-peptidergic afferents, at the L4–L5 spinal levels, is not sufficient to trigger the de novo expression of NK-1r by projection pyramidal neurons but increases the expression of NK-1r in fusiform and multipolar projection neurons. Furthermore, our data suggest that a neuropathic component is essential to trigger the expression of NK-1r by pyramidal neurons. (Source: Molecular Pain)
Source: Molecular Pain - September 9, 2015 Category: Molecular Biology Authors: Abeer SaeedSophie PawlowskiAlfredo Ribeiro-da-Silva Source Type: research
Leukotriene enhances NMDA-induced inward currents in dorsal horn neurons of the rat spinal cord after peripheral nerve injury
Conclusion:
Our findings showed that LTB4, which may originate from microglia, can activate BLT1 receptors which are expressed on the membrane of spinal dorsal horn neurons during neuropathic pain. This glia-neuron interaction induces the enhancement of NMDA currents through intracellular G-proteins. The enhancement of NMDA receptor sensitivity of dorsal horn neurons may lead to central sensitization, leading to mechanical pain hypersensitivity. (Source: Molecular Pain)
Source: Molecular Pain - September 9, 2015 Category: Molecular Biology Authors: Yasukuni KiyoyukiWataru TaniguchiMasamichi OkuboHiroki YamanakaKimiko KobayashiNaoko NishioTerumasa NakatsukaKoichi Noguchi Source Type: research
