Chunk #38 — Nicotine and ethanol: nAChR-mediated neurotransmission and plasticity — Amygdala and hippocampal complex: learning and memory — Hippocampus
(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 al., 2001; Ge and Dani, 2005). Furthermore, activation of α7 nAChRs on pre-synaptic glutamatergic terminals can increase the frequency of miniature EPSCs and enhance glutamate release onto pyramidal neurons offering yet another mechanism for the modulation of plasticity (Gray et al., 1996; Radcliffe and Dani, 1998). In the CA3 region of hippocampal slices, bath application of nicotine can drive the pyramidal cells above threshold in the absence of an action potential by activating pre-synaptic nAChRs located on glutamatergic terminals. Activation of these receptors enhances miniature EPSCs and glutamate release through mobilization of intracellular calcium stores by CICR (Sharma and Vijayaraghavan, 2003).
