At the cellular level, neuronal activity in the hippocampus is strongly modulated by both nAChRs and mAChRs. Cholinergic inputs to the hippocampus from the medial septum and the diagonal band of Broca impinge on both glutamatergic and GABAergic neurons throughout the structure, and a comprehensive review of the effects of ACh on synaptic plasticity in the hippocampus has been published recently (Drever et al., 2011). The ability of ACh to induce synaptic plasticity through actions on pre- and post-synaptic nAChRs and mAChRs is likely to modulate learning and memory, including memory of stressful events (Nijholt et al., 2004), and a role for ACh in regulation of hippocampal excitability through presynaptic release of glutamate and GABA has also been well-characterized (Alkondon et al., 1997; Freund et al., 1988; Radcliffe et al., 1999). Stress also induces alternative splicing of the AChE mRNA in the hippocampus leading to altered ACh signaling in this structure (Nijholt et al., 2004). There is currently no consensus on how these cholinergic actions converge to regulate the output of the hippocampus in response to stress, although one possibility
