Abstract
Wild-type and α5 null mutant mice were used to identify nicotinic cholinergic receptors (nAChRs) that mediate α-conotoxin MII (α-CtxMII)-resistant dopamine (DA) release from striatal synaptosomes. Concentration–effect curves for ACh-stimulated release (20 s) were monophasic when wild-type synaptosomes were assayed but biphasic with synaptosomes from the α5 null mutant. Deleting the α5 gene also resulted in decreased maximal ACh-stimulated α-CtxMII-resistant DA release. When a shorter perfusion time (5 s) was used, biphasic curves were detected in both wild-type and α5 null mutants, indicative of high- and low-sensitivity (HS and LS) activity. In addition, DHβE-sensitive (HS) and DHβE-resistant (LS) components were found in both genotypes. These results indicate that α-CtxMII-resistant DA release is mediated by α4α5β2, (α4)2(β2)3 (HS), and (α4)3(β2)2 (LS) nAChRs.
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Proceedings of the XIII International Symposium on Cholinergic Mechanisms
Supported by NIH grants DA003194 and DA015663 (to A.C.C), DA012242 (to M.J.M. and J.M.M.), MH53631, and GM48677 (to J.M.M.).
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Grady, S.R., Salminen, O., McIntosh, J.M. et al. Mouse Striatal Dopamine Nerve Terminals Express α4α5β2 and Two Stoichiometric Forms of α4β2*-Nicotinic Acetylcholine Receptors. J Mol Neurosci 40, 91–95 (2010). https://doi.org/10.1007/s12031-009-9263-y
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DOI: https://doi.org/10.1007/s12031-009-9263-y