Literature DB >> 14622196

Differential contributions of the basolateral and central nuclei of the amygdala in the negative affective component of chemical somatic and visceral pains in rats.

Sachi Tanimoto1, Takayuki Nakagawa, Yosuke Yamauchi, Masabumi Minami, Masamichi Satoh.   

Abstract

Pain is a multidimensional conscious experience including sensory and negative affective components. The neural systems of the sensory component of pain have been extensively studied, while those of the negative affective component are less clear. The amygdala is a forebrain structure composed of several distinct nuclei including the basolateral (BLA) and central (CeA) nuclei, and is thought to be a key neural substrate underlying emotional responses. Recently, we reported that intraplantar (i.pl.) injection of formalin as a chemical somatic noxious stimulus increased c-fos mRNA expression in the BLA, but not CeA, while intraperitoneal (i.p.) injection of acetic acid as a chemical visceral noxious stimulus induced it highly in the CeA, and hardly in BLA [Nakagawa et al. (2003) Neurosci. Lett., 344, 197-200]. In this study, we examined the effects of discrete bilateral excitotoxic lesions of the BLA or CeA on the sensory and negative affective components of the two types of pain in Sprague-Dawley rats. In the place-conditioning paradigm, both i.pl. formalin and i.p. acetic acid produced conditioned place aversion. The i.pl. formalin-induced conditioned place aversion was abolished by the lesion of the BLA or CeA, while the i.p. acetic acid-induced conditioned place aversion was abolished by the CeA-, but not BLA-lesion. On the other hand, the BLA- or CeA-lesion failed to reduce the i.pl. formalin- and i.p. acetic acid-produced nociceptive behaviours. Taken together, these results suggest that activation of distinct amygdaloid nuclei could differentially contribute to chemical somatic and visceral noxious stimuli-induced negative affective, but not sensory components of pains.

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Year:  2003        PMID: 14622196     DOI: 10.1046/j.1460-9568.2003.02952.x

Source DB:  PubMed          Journal:  Eur J Neurosci        ISSN: 0953-816X            Impact factor:   3.386


  55 in total

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