Chunk #37 — Nicotine and ethanol: nAChR-mediated neurotransmission and plasticity — Amygdala and hippocampal complex: learning and memory — Hippocampus
nAChR-mediated synaptic plasticity. Nicotinic receptors exert a temporally- and spatially-dependent bidirectional control over synaptic plasticity, both in vitro and in vivo (Table 2). For example, in the CA1 region of hippocampal slices ACh and nicotine can act on post-synaptic receptors of pyramidal neurons to increase intracellular Ca2+ which facilitates the conversion of short-term potentiation to LTP by reducing the threshold needed for induction (Fujii et al., 1999; Ji and Dani, 2000; Nakauchi et al., 2007) or by attenuating the inhibitory input of interneurons to pyramidal cells (Ji and Dani, 2000; Yamazaki et al., 2005); these effects are mediated by both the activation of non-α7 nAChRs and the inactivation of α7 nAChRs (Fujii et al., 2000a). Furthermore, blunting the evoked release of inhibitory GABA onto pyramidal cells to facilitate nicotine-induced LTP induction was shown to rely on desensitization of non-α7 nAChRs (Fujii et al., 2000b; Yamazaki et al., 2005; Nakauchi et al., 2007). Additionally, activation of nAChRs on hippocampal interneurons can induce LTP or LTD depending on the exact timing of agonist application in respect to the pre-synaptic stimulation (Ji et
