Functional nAChRs expressed on pyramidal cells (somato-dendritic α7), GABAergic interneurons (α7, α4β2*, and α3β4*), and glutamatergic afferents (α7) modulate synaptic transmission in the amygdala (see Figure 3) (Hill et al., 1993; Perry et al., 2002; Klein and Yakel, 2006). Whole cell patch-clamp recordings demonstrated nicotine increases the frequency of both glutamatergic and GABAergic spontaneous post synaptic currents (PSCs) and this effect was sensitive to the α7-selective antagonist α-bungarotoxin, thus implicating a role of pre-synaptic α7 nAChRs (Barazangi and Role, 2001). Another report showed that activation of predominately α3β4* nAChRs on GABAergic interneurons in the basolateral nucleus of the amygdala were responsible for the enhanced frequency of inhibitory PSCs (Zhu et al., 2005).
