Glucocorticoids enhance the excitability of principal basolateral amygdala neurons.

A large body of pharmaco-behavioral data implicates the basolateral nucleus of the amygdala (BLA) in the facilitation of memory consolidation by emotions. Overall, this evidence suggests that stress hormones released during emotional arousal increase the activity of BLA neurons. In turn, this increased BLA activity would facilitate synaptic plasticity elsewhere in the brain, to which the BLA projects. However, the direct effects of glucocorticoids on BLA neurons are incompletely understood. In the present study, we examined the direct effects of corticosterone (CORT) on principal neurons of the rat BLA in vitro using whole-cell patch-clamp recordings. We found that application of a stress level of CORT for 20 min caused significant changes in the passive properties and responsiveness of BLA cells measured 1-2 h later. Indeed, CORT application produced a depolarization of the resting potential, an increase in input resistance, and a dramatic decrease in spike-frequency adaptation. In addition, GABA(A) IPSPs evoked by stimulation of the external capsule were significantly reduced by CORT application. This effect of CORT was not attributable to a reduction in the amount of GABA released because GABA(B) IPSPs were unchanged and the resistance drop associated with GABA(A) IPSPs was not altered. Rather, we found that this effect of CORT resulted from a positive shift of the GABA(A) reversal potential. Overall, these results suggest that, in agreement with previous behavioral findings, glucocorticoids enhance the excitability of principal BLA cells by increasing their intrinsic excitability and decreasing the impact of GABA(A) IPSPs.