BLA pyramidal neurons influence physiological, hormonal, and behavioral responses to stress in part through excitatory projections to the central extended amygdala, prefrontal cortex, and striatum (Sah et al, 2003). The spontaneous activity of these neurons is maintained at low levels by high local GABAergic inhibitory tone. Impairments in GABAergic transmission within the BLA have been suggested to contribute to anxiety and affective disorders (Quirk and Gehlert, 2003). CB1 receptors inhibit local GABAergic transmission within the BLA (Azad et al, 2003; Katona et al, 2001), an effect that likely contributes to the anxiogenic effects of high-dose exogenous cannabinoids (Patel et al, 2005a). Our data indicate that repeated stress enhances the ability of BLA neurons to engage in DSI, a form of short-term activity-dependent neuroplasticity that could enhance persistent firing of principle neurons (Carter and Wang, 2007). These data suggest that stress-induced enhancement in eCB signaling could result in increased activity of BLA pyramidal neurons, and contribute to the expression of physiological and behavioral responses to repeated stress. However, CB1 receptors also modulate excitatory transmission in the BLA (Azad et al, 2003),
