NDLI: Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury.

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Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury.

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Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Guixia Wu, Chunfu Li, Chunli Liu, Xifang She, Fenglin Chen, Jianzhao Du, Jingnan
Description	Author Affiliation: Li G ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); Liu X ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); Du J ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); Chen J ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); She F ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); Wu C ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.); Li C ( Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, P.R. China.)
Abstract	Neuropathic pain is a global medical concern, characterized by spontaneous pain, heat hyperalgesia and mechanical allodynia. The condition has been associated with alterations in the voltagegated sodium channels, Nav1.8 and Nav1.9, in nociceptive neurons termed nociceptors. However, an explanation for the contribution of these channels to the phenotype observed in neuropathic pain remains to be elucidated. The changes induced by chronic constriction injury (CCI) to Nav1.8 and Nav1.9 mRNA and protein levels, as well as electrical currents in injured and contralateral noninjured dorsal root ganglion (DRG) neurons are described in the present study. A marked downregulation was observed for each Nav isoform transcript and protein expressed in injured neurons with the exception of the Nav1.9 protein, which exhibited no change, while in contralateral noninjured neurons, the levels of protein and mRNA remained unchanged. Nav isoform functional analysis was then performed in L(46) DRG neurons 14 days after CCI. The Nav1.8 current density was markedly decreased in injured DRG neurons following CCI. The voltagedependent activation of the Nav1.8 channel in these neurons was shifted to depolarized potentials by 5.3 mV, while it was shifted to hyperpolarized potentials by 10 mV for inactivation. The electrophysiological function of Nav1.9 was not affected by CCI. The present study demonstrated that ectopic discharge following CCI, which was likely induced by a positive shift in the Nav1.8 current inactivation curve in injured neurons, enhanced the excitability of the neurons by facilitating tetrodotoxinresistant sodium channels into the fast inactivation state and did not occur as a result of a compensatory redistribution in the contralateral uninjured neurons.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	12
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-09-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Ganglia, Spinal Pathology Nav1.8 Voltage-gated Sodium Channel Metabolism Neuralgia Neurons Action Potentials Animals Constriction Hyperalgesia Etiology Genetics Nav1.9 Voltage-gated Sodium Channel Complications Rna, Messenger Rats, Sprague-dawley Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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