Chunk #39 — Nicotine and ethanol: nAChR-mediated neurotransmission and plasticity — Amygdala and hippocampal complex: learning and memory — Hippocampus
Within the dentate gyrus, induction of LTP by nicotine required activation of mGLuR5 and L-type Ca2+ channels, as well as Ca2+ release from ryanodine-sensitive stores and was α7 nAChR-dependent (Welsby et al., 2006, 2009). in vivo studies in mice showed nicotine or epibatidine, an α4β2 nAChR agonist, dose-dependently induced synaptic plasticity in the dentate gyrus and importantly, required intact midbrain DA signaling (Matsuyama et al., 2000; Matsuyama and Matsumoto, 2003; Tang and Dani, 2009). In the developing brain, long-lasting changes in synaptic transmission were observed following a single exposure to nicotine in the hippocampus. nAChR signaling facilitated the conversion of pre-synaptic silent synapses into functional ones and was shown to be dependent on α7 nAChRs most likely localized on pre-synaptic glutamatergic nerve endings (Maggi et al., 2003). Together these findings strongly imply that the timing and location of nAChR activity are important determinants for synaptic plasticity in the hippocampus.
