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Molecular Pharmacology

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Research ArticleArticle

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

Sergio Kaiser and Susan Wonnacott
Molecular Pharmacology August 2000, 58 (2) 312-318; DOI: https://doi.org/10.1124/mol.58.2.312
Sergio Kaiser
Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom
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Susan Wonnacott
Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom
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Abstract

Nicotinic agonists elicit the release of dopamine from striatal synaptosomes by acting on presynaptic nicotinic acetylcholine receptors (nAChRs) on dopamine nerve terminals. Both α3β2* and α4β2 nAChR subtypes (but not α7* nAChRs) have been implicated. Here, we compared nAChR-evoked [3H]dopamine release from rat striatal synaptosome and slice preparations by using the nicotinic agonist anatoxin-a. In the more integral slice preparation, the concentration-response curve for anatoxin-a-evoked [3H]dopamine release was best fitted to a two-site model, giving EC50 values of 241 nM and 5.1 μM, whereas only the higher-affinity component was observed in synaptosome preparations (EC50 = 134 nM). Responses to a high concentration of anatoxin-a (25 μM) in slices (but not in synaptosomes) were partially blocked by ionotropic glutamate receptor antagonists (kynurenic acid, 6,7-dinitroquinoxaline-2,3-dione) and by α7*-selective nAChR antagonists (α-bungarotoxin, α-conotoxin-ImI, methyllycaconitine) in a nonadditive manner. In contrast, the α3β2-selective nAChR antagonist α-conotoxin-MII partially inhibited [3H]dopamine release from both slice and synaptosome preparations, stimulated with both low (1 μM) and high (25 μM) concentrations of anatoxin-a. Antagonism by α-conotoxin-MII was additive with that of α7*-selective antagonists. These data support a model in which α7* nAChRs on striatal glutamate terminals elicit glutamate release, which in turn acts at ionotropic glutamate receptors on dopamine terminals to stimulate dopamine release. In addition, non-α7* nAChRs on dopamine terminals also stimulate dopamine release. These observations have implications for the complex cholinergic modulation of inputs onto the major efferent neurons of the striatum.

Footnotes

    • Received March 13, 2000.
    • Accepted May 8, 2000.
  • Send reprint requests to: Dr. S. Wonnacott, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK. E-mail: s.wonnacott{at}bath.ac.uk

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

  • This work was supported by grants from the Biological and Biotechnological Sciences Research Council and European Community.

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 58 (2)
Molecular Pharmacology
Vol. 58, Issue 2
1 Aug 2000
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Research ArticleArticle

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

Sergio Kaiser and Susan Wonnacott
Molecular Pharmacology August 1, 2000, 58 (2) 312-318; DOI: https://doi.org/10.1124/mol.58.2.312

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Research ArticleArticle

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

Sergio Kaiser and Susan Wonnacott
Molecular Pharmacology August 1, 2000, 58 (2) 312-318; DOI: https://doi.org/10.1124/mol.58.2.312
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