et al., 1996). For instance, hippocampal and cortical ACh levels can increase following restraint stress in rats, while ACh levels in the amygdala are unchanged, although an increase in amygdalar cholinergic tone can also reduce BLA activity though activation of mAChRs (Power and Sah, 2008). Conversely, acute activation of presynaptic α7 nAChRs in the BLA can also favor the release of glutamate from impinging cortical projections, which is critical for aversive memory and fear (Klein and Yakel, 2006). Stimulation of this pathway during development blunts paired facilitation due to subsequent stimulation, however, which would be expected to decrease BLA reactivity (Jiang and Role, 2008), further highlighting the role of cholinergic signaling in plasticity of this system. The hippocampus provides inhibitory feedback to the amygdala through inhibition of the hypothalamic-pituitary-adrenal (HPA) axis (Tasker and Herman, 2011). Interestingly, relief from stress leads to an increase in cholinergic signaling in the amygdala and PFC (Mark et al., 1996), indicating that the valence of ACh varies by brain area. The effect of increased cortical ACh levels on amygdala signaling has not been studied, but stress impairs PFC output (Arnsten, 2009), and PFC can normally decrease basolateral amygdala activity through projections to the intercalated nucleus
