The amygdala also receives cholinergic inputs from the basal forebrain complex (Mesulam, 1995) and is consistently hyperactivated in fMRI studies of patients with mood disorders (Drevets, 2001). In rodents, decreasing ACh signaling through nAChRs depresses neuronal activity in the basolateral amygdala as measured by c-fos immunoreactivity (Mineur et al., 2007). As discussed above, ACh shapes the output of cortical neurons, and cortico-amygdala glutamatergic connections are also strongly and persistently potentiated by nAChR stimulation (Mansvelder et al., 2009). Thus, ACh release in the amygdala is thought to strengthen associations between environmental stimuli and stressful events, potentially contributing to maladaptive learning underlying affective disorders (Mansvelder et al., 2009).
