The change of HCN1/HCN2 mRNA expression in peripheral nerve after chronic constriction injury induced neuropathy followed by pulsed electromagnetic field therapy.

Hui Liu,Yunxia Zuo,Lianbing Gu,Jun Zhou

doi:10.18632/oncotarget.13584

Hui Liu, Yunxia Zuo + Show 2 more

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https://doi.org/10.18632/oncotarget.13584

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Journal: Oncotarget	Publication Date: Nov 25, 2016
Citations: 23	License type: cc-by

Affiliation: Sichuan University, Jiangsu Cancer Hospital

Abstract

Neuropathic pain is usually defined as a chronic pain state caused by peripheral or central nerve injury as a result of acute damage or systemic diseases. It remains a difficult disease to treat. Recent studies showed that the frequency of action potentials in nociceptive afferents is affected by the activity of hyperpolarization-activated cyclic nucleotide-gated cation channels (HCN) family. In the current study, we used a neuropathy rat model induced by chronic constriction injury (CCI) of sciatic nerve to evaluate the change of expression of HCN1/HCN2 mRNA in peripheral nerve and spinal cord. Rats were subjected to CCI with or without pulsed electromagnetic field (PEMF) therapy. It was found that CCI induced neural cell degeneration while PEMF promoted nerve regeneration as documented by Nissl staining. CCI shortened the hind paw withdrawal latency (PWL) and hind paw withdrawal threshold (PWT) and PEMF prolonged the PWL and PWT. In addition, CCI lowers the expression of HCN1 and HCN2 mRNA and PEMF cannot restore the expression of HCN1 and HCN2 mRNA. Our results indicated that PEMF can promote nerve regeneration and could be used for the treatment of neuropathic pain.

Highlights

Neuropathic pain is usually defined as a chronic pain state caused by peripheral or central nerve injury as a result of acute damage or systemic diseases
These results indicated that constriction injury (CCI) shorten the paw withdrawal latency (PWL) and pulsed electromagnetic field (PEMF) can promote the recovery of injury and prolong the PWL to thermal stimulation
Our study revealed the change of expression of HCN1/HCN2 mRNA in the left/right sciatic nerve, left/ right dorsal root ganglion (DRG) and spinal cord after CCI induced neuropathy

Summary

Introduction

Neuropathic pain is usually defined as a chronic pain state caused by peripheral or central nerve injury as a result of acute damage or systemic diseases. It is characterized by unpleasant abnormal sensation (dysesthesia), increased response to painful stimuli (hyperalgesia) and pain in response to a stimulus that does not normally provoke pain (allodynia) [1]. HCN represents the molecular correlation of Ih current, a cation current activated by membrane hyperpolarization contributing to the formation of resting membrane potential. All four HCN members (HCN1, HCN2, HCN3 and HCN4) have been found in central and peripheral nervous system, where they are associated with synaptic integration, neuronal excitability and the formation of resting membrane potentials [3]. HCN1 and HCN2 are the most expressed isoforms in primary somatosensory neurons [4; 5]

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