GABAA receptors in the central nucleus of amygdala (CeA) affect on pain modulation

Abstract

The central nucleus of the amygdala (CeA), the nociceptive amygdala, serves as the major output nucleus of the amygdala and participates in receiving and processing pain information. Considering the abundance of GABAA receptors in the CeA and also the attributed bidirectional roles for GABA in controlling nociception, we examined the effects of bilateral intra-CeA microinjection of a different dose of the GABAA receptor agonist, muscimol, and the GABAA receptor antagonist, bicuculline, on pain modulation using a tail-flick test. Adult rats were exposed to intra-CeA microinjection of a selective GABAA receptor antagonist, bicuculline, (50,100,200,400 ng/side) or a selective GABAA receptor agonist, muscimol, (62.5, 125,250,500 ng/side) and subjected to the tail-flick test. Tail-flick latencies were measured every 5 min after drug microinjection for 60 min. Microinjection of bicuculline and muscimol into the CeA increased and decreased tail-flick latency, respectively in a dose-dependent fashion. The hyperalgesic effect of muscimol (500 ng) microinjected into the CeA was attenuated (P<0.001) by a prior microinjection of bicuculline (50 ng) at the same site. The results of the present study showed that locally released GABA in the CeA is involved in pain modulation and suggests the existence of a GABAA mediated inhibitory system in the CeA on pain control.