Basolateral amygdala lesion inhibits the development of pain chronicity in neuropathic pain rats.

Zheng Li,Jing Wang,Lin Chen,You Wan,Meng Zhang,Theodore John Price

doi:10.1371/journal.pone.0070921

Abstract

BackgroundChronicity of pain is one of the most interesting questions in chronic pain study. Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain. The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information.ObjectiveThis study aimed to investigate whether amygdala or its subregions, the basolateral amygdala (BLA) and the central medial amygdala (CeA), contributes to the pain chronicity in the spared nerve injury (SNI)-induced neuropathic pain model of rats.Methodology/Principal Findings(1) Before the establishment of the SNI-induced neuropathic pain model of rats, lesion of the amygdaloid complex with stereotaxic injection of ibotenic acid (IBO) alleviated mechanical allodynia significantly at days 7 and 14, even no mechanical allodynia at day 28 after SNI; Lesion of the BLA, but not the CeA had similar effects; (2) however, 7 days after SNI when the neuropathic pain model was established, lesion of the amygdala complex or the BLA or the CeA, mechanical allodynia was not affected.ConclusionThese results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity.

Highlights

Neuropathic pain is a kind of chronic pain resulting from injury of somatosensory system
Methodology/Principal Findings: (1) Before the establishment of the spared nerve injury (SNI)-induced neuropathic pain model of rats, lesion of the amygdaloid complex with stereotaxic injection of ibotenic acid (IBO) alleviated mechanical allodynia significantly at days 7 and 14, even no mechanical allodynia at day 28 after SNI; Lesion of the basolateral amygdala (BLA), but not the central medial amygdala (CeA) had similar effects; (2) 7 days after SNI when the neuropathic pain model was established, lesion of the amygdala complex or the BLA or the CeA, mechanical allodynia was not affected. These results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity
In the sham SNI rats with IBO lesion or with sham lesion, paw withdrawal threshold (PWT) had no significant difference at all time points (p.0.05), indicating that amygdala lesion had no effect on basal pain threshold.In the SNI rats, before the SNI surgery, there is no significant difference between PWTs in the SNI rats with IBO lesion or with sham lesion (p.0.05)

Summary

Introduction

Neuropathic pain is a kind of chronic pain resulting from injury of somatosensory system. It is characterized by pain persistence even after original damages have been recovered [1]. Chronic pain is a process that develops from somatosensory nerve injury and maintains. Clinical data demonstrate that negative emotions such as depression and anxiety are high risk factors in the development of chronic pain, and promote transition from acute pain to chronic pain [5]. It is reasonable to speculate that supraspinal brain regions which process negative emotional information probably contribute to pain chronicity or facilitate the development of chronic pain. Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain. The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information

Methods

Results

Conclusion