Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas.

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Guidelines on nicotine dose selection for in vivo research (2007, background): “Dihydro-β-erythroidine (DHβE) is more selective for the widespread α4β2* nAChRs (Mansvelder et al. 2002), whereas α-conotoxin MII is the preferred antagonist for nAChRs containing α6 or α3 subunits (Kulak et al. 2002; Whiteaker et al. 2000a, b), central to the mesocorticolimbic reward pathway.”
Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function (2009, background): “Activation of α4β2 nAChRs on GABAergic interneurons in the VTA relieves the inhibitory control they exert on dopaminergic neurons (295,380).”
Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior (2012, background): “Nicotinic modulation of neurotransmitter release is often subtypespecific, and this specificity can vary across brain areas, with distinct nAChRs coupling to release of glutamate (a7) versus GABA (a4b2) (Mansvelder et al., 2002) in the ventral tegmental area (VTA), while b2-containing nAChRs can mod”
Getting formal with dopamine and reward. (2002, neutral): “(see above) and thus are particularly amenable for en- hancement by reuptake blockade, as they are faster and reach their peaks before most negative feedback higher levels of excitability (Mansvelder et al., 2002).becomes effective.”