Central nucleus of the amygdala and the control of tonic immobility in guinea pigs

Abstract

Tonic immobility (TI) is a temporary state of profound motor inhibition induced by situations that supposedly generate intense fear, with the objective to protect the animal from attacks by predators. A previous study by our group demonstrated that cholinergic stimulation of the central, basolateral, and lateral posterior nuclei of the amygdala decreases the duration of TI in guinea pigs. In the current study, we attempted to investigate the effects of cholinergic, opioidergic, and γ-aminobutyric acid (GABA)ergic stimulation of the central amygdala (CEA) on TI modulation. We observed that both cholinergic (carbachol, 2.7 nmol/0.2 μl) and opioidergic (morphine, 2.2 and 4.4 nmol/0.2 μl) stimulation of the CEA decreased the duration of TI and that these effects could be reversed by pretreatment with naloxone (1.3 and 2.7 nmol/0.2 μl). Our results also showed that microinjection of the GABAergic agonist muscimol (0.26 nmol/0.2 μl) reduced the duration of TI episodes, whereas microinjection of the GABAergic antagonist bicuculline (BIC, 1 nmol/0.2 μl) increased it. Thus, the present experiments demonstrated that cholinergic, opioidergic, and GABAergic systems of the CEA have an inhibitory action on the duration of TI in guinea pigs. Furthermore, the current study suggests an interaction of cholinergic and opioidergic mechanisms. In addition, the GABAergic circuit of the CEA has a tonic inhibitory influence on the duration of TI and is mediated by GABA A receptors.