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Volume 17, Number 14,
Issue of July 15, 1997
pp. 5263-5270
Copyright ©1997 Society for Neuroscience
 -Conotoxin MII Blocks
Nicotine-Stimulated Dopamine Release in Rat Striatal Synaptosomes
Received March 11, 1997; revised April 8, 1997; accepted April 23, 1997.
Jennifer M. Kulak1,
Thu A. Nguyen1,
Baldomero M. Olivera1, and
J. Michael McIntosh1, 2
Departments of 1 Biology and 2 Psychiatry,
University of Utah, Salt Lake City, Utah, 84112
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  3/ 2 subunit
interface.
The recently discovered peptide -conotoxin MII is a
potent and selective inhibitor of rat nAChRs containing an interface formed by 3 and 2 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 -conotoxin MII, namely -conotoxin
MI (selective for 11  nAChRs) and -conotoxin ImI (selective for 7-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 3/2 subunit interface. In contrast,
 10% of nicotine-stimulated release of norepinephrine from
hippocampal synaptosomes is modulated by nAChRs with 3/2 subunit
interfaces.
Key words:
-conotoxin MII;
dopamine release;
striatum;
nicotine;
32 receptor;
acetylcholine;
norepinephrine
release;
hippocampus
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