nAChR-mediated synaptic plasticity. In the amygdala (Table 2), nicotine has been shown to facilitate LTP in a pathway-specific manner. Robust LTP in amygdala slices from mice that received nicotine treatment for 7 days compared to controls and persisted 72 h after nicotine cessation. Even just one day of nicotine exposure significantly enhanced LTP. The nicotine-induced facilitation of LTP was found to be dependent on both α7 and β2-containing nAChRs and at least partially, to activation of nAChRs on GABAergic interneurons that ultimately reduce inhibition of pyramidal neurons. Furthermore, LTP was completely blocked by D-APV, an NMDAR antagonist, demonstrating the essential role of NMDARs in nicotine-mediated plasticity in the amygdala. The authors suggest that as seen in other brain regions, nicotine may also be acting on pre-synaptic nAChRs on glutamatergic terminals to enhance glutamate release or increasing postsynaptic Ca2+ influx through voltage-dependent calcium channels (Huang et al., 2008). At this time, little is known about nicotinic receptor-mediated plasticity in the amygdala. Ethanol is capable of modulating synaptic changes in this circuit but it has yet to be elucidated if and how nicotinic receptors are involved.
