alpha -Bungarotoxin-Sensitive Nicotinic Receptors Indirectly Modulate [3H]Dopamine Release in Rat Striatal Slices via Glutamate Release

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Vol. 58, Issue 2, 312-318, August 2000

$alpha$ -Bungarotoxin-Sensitive Nicotinic Receptors Indirectly Modulate [³H]Dopamine Release in Rat Striatal Slices via Glutamate Release

Sergio Kaiser¹ and Susan Wonnacott

Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom

Nicotinic agonists elicit the release of dopamine from striatal synaptosomes by acting on presynaptic nicotinic acetylcholinereceptors (nAChRs) on dopamine nerve terminals. Both $alpha$ 3 $beta$ 2* and $alpha$ 4 $beta$ 2 nAChR subtypes (but not $alpha$ 7* nAChRs) have been implicated.Here, we compared nAChR-evoked [³H]dopamine release from rat striatal synaptosome and slice preparationsby using the nicotinic agonist anatoxin-a. In the more integralslice preparation, the concentration-response curve for anatoxin-a-evoked[³H]dopamine release was best fitted to a two-site model, givingEC₅₀ values of 241 nM and 5.1 µM, whereas only the higher-affinitycomponent was observed in synaptosome preparations (EC₅₀ = 134nM). Responses to a high concentration of anatoxin-a (25 µM) inslices (but not in synaptosomes) were partially blocked by ionotropicglutamate receptor antagonists (kynurenic acid, 6,7-dinitroquinoxaline-2,3-dione)and by $alpha$ 7*-selective nAChR antagonists ( $alpha$ -bungarotoxin, $alpha$ -conotoxin-ImI,methyllycaconitine) in a nonadditive manner. In contrast, the $alpha$ 3 $beta$ 2-selective nAChR antagonist $alpha$ -conotoxin-MII partially inhibited[³H]dopamine release from both slice and synaptosome preparations,stimulated with both low (1 µM) and high (25 µM) concentrationsof anatoxin-a. Antagonism by $alpha$ -conotoxin-MII was additive withthat of $alpha$ 7*-selective antagonists. These data support a modelin which $alpha$ 7* nAChRs on striatal glutamate terminals elicit glutamaterelease, which in turn acts at ionotropic glutamate receptorson dopamine terminals to stimulate dopamine release. In addition,non- $alpha$ 7* nAChRs on dopamine terminals also stimulate dopamine release.These observations have implications for the complex cholinergicmodulation of inputs onto the major efferent neurons of thestriatum.

¹ Present address: Department of Biology, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0357.

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