Abstract

To study the effects of acupuncture analgesia on the hippocampus, we observed the effects of electroacupuncture (EA) and mitogen-activated protein kinase (MEK) inhibitor on pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the hippocampal area CA1 of sham or chronic constrictive injury (CCI) rats. The animals were randomly divided into a control, a CCI, and a U0126 (MEK1/2 inhibitor) group. In all experiments, we briefly (10-second duration) stimulated the sciatic nerve electrically and recorded the firing rates of PENs and PINs. The results showed that in both sham and CCI rats brief sciatic nerve stimulation significantly increased the electrical activity of PENs and markedly decreased the electrical activity of PINs. These effects were significantly greater in CCI rats compared to sham rats. EA treatment reduced the effects of the noxious stimulus on PENs and PINs in both sham and CCI rats. The effects of EA treatment could be inhibited by U0126 in sham-operated rats. The results suggest that EA reduces effects of acute sciatic nerve stimulation on PENs and PINs in the CA1 region of the hippocampus of both sham and CCI rats and that the ERK (extracellular regulated kinase) signaling pathway is involved in the modulation of EA analgesia.

Highlights

  • Peripheral nerve injuries produce acute pain and often induce neuropathic pain, a severe clinical problem and chronic debilitating condition that affects the nervous system

  • Neuropathic pain induced hippocampal interleukin-1 beta (IL-1β) mRNA levels upregulation, and the changes of IL1β mRNA expression correlated with the injured side of the hippocampus [6]

  • On the basis of these studies, the objective of this research is to investigate the effects of EA and the extracellular regulated protein kinases (ERK) signaling pathway on the acute pain-induced responses of pain-related neurons in the hippocampus of Wistar rats under both control and neuropathic pain conditions

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Summary

Introduction

Peripheral nerve injuries produce acute pain and often induce neuropathic pain, a severe clinical problem and chronic debilitating condition that affects the nervous system. Neuropathic pain is relatively common and impairs the quality of life of sufferers. Chronic constrictive injury (CCI) has been the common neuropathic pain model since 1988 [1, 2]. The hippocampus, a part of the limbic system, has the function of learning, memory, emotion, and affect and has relationships with chronic and acute pain. Humans suffering from chronic or severe pain had smaller hippocampal volumes. Hippocampal N-acetylaspartate/creatine decreased in elderly patients suffering from acute pain [4, 5]. Neuropathic pain induced hippocampal interleukin-1 beta (IL-1β) mRNA levels upregulation, and the changes of IL1β mRNA expression correlated with the injured side of the hippocampus [6]. Xiao et al [7], Yang et al [8], and Li et al [9]

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