The hippocampus and amygdala have been implicated in mediating some of the cognitive-enhancing effects of nicotine, supported by findings that show microinfusion of nAChR agonists can enhance memory-related functions, while antagonists impair them (Ohno et al., 1993; Felix and Levin, 1997). For example, direct infusion of nicotine into basolateral nucleus of the amygdala enhanced working memory and facilitated the acquisition and consolidation of short- and long-term memories; on the other hand, infusion of MLA had opposite effects on memory performance (Barros et al., 2005). Microinfusion of DHβE or MLA into basolateral nucleus of rats resulted in working memory deficits in the radial-arm maze, indicating both α7 and α4β2* nAChRs in this area are involved in normal memory function (Addy et al., 2003). In addition, nicotine dose-dependently stimulates the release of norepinephrine in the amygdala and hippocampus by activating nAChRs localized on norepinephrinergic neurons in the brainstem (Fu et al., 1998). Norepinephrine contributes to memory function and the stress response (Liang et al., 1990; Bremner et al., 1996), offering yet another mechanism by which nicotine modulates these processes.
