There is experimental evidence illustrating nicotine-induced plasticity (Table 1) in VTA slice preparations where application of nicotine (500 nM) was shown to increase the AMPA/NMDA receptor ratio by increasing pre-synaptic release of glutamate. This effect is mediated by α7 nAChRs since pre-incubation with the α7 antagonist (MLA), but not the β2*-antagonist (DHβE), abolished the nicotine-induced LTP. In support, α7 knockout mice lack this response to nicotine (Jin et al., 2011). Furthermore, the nicotine-induced enhancement of excitatory currents lasts after prolonged exposure suggesting a lack of α7 desensitization (Pidoplichko et al., 2004) and persists even after nicotine is removed from the bath, thereby indicating LTP (Mansvelder and McGehee, 2000; Dani, 2001; Mansvelder et al., 2002).
