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Activation of presynaptic nicotinic acetylcholine receptors (nAChRs) can induce the release of neurotransmitters such as dopamine and norepinephrine in the CNS. Accumulating evidence suggests that distinct nAChR subtypes are involved; however, it has been difficult to determine the subunit composition of these receptors, in part because of the lack of a sufficient variety of selective nAChR ligands. We present experimental data that at least two different nAChR complexes are involved in dopamine release, one of which has an α3/β2 subunit interface. The recently discovered peptide α-conotoxin MII is a potent and selective inhibitor of rat nAChRs containing an interface formed by α3 and β2 subunits. We used this peptide to examine nicotine-stimulated release of dopamine from rat striatal synaptosomes and of norepinephrine from hippocampal synaptosomes. MII (100 nm) blocks 34–49% of the nicotine-stimulated dopamine release, but not dopamine release evoked by elevated [K+]. Furthermore, two peptides structurally related to α-conotoxin MII, namely α-conotoxin MI (selective for α1β1γδ nAChRs) and α-conotoxin ImI (selective for α7-containing nAChRs), have no effect on nicotine-stimulated dopamine release. The results indicate that one third to half of the dopamine release in the striatal preparation is mediated by nAChRs with an α3/β2 subunit interface. In contrast, ≤10% of nicotine-stimulated release of norepinephrine from hippocampal synaptosomes is modulated by nAChRs with α3/β2 subunit interfaces.

α-Conotoxin MII Blocks Nicotine-Stimulated Dopamine Release in Rat Striatal Synaptosomes