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Nicotine indirectly increases acetylcholine release in rat striatum
Author(s) -
Machová E.,
Žemličková V.,
Doležal V.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.15_3.x
Subject(s) - mecamylamine , nicotine , glutamatergic , acetylcholine , nicotinic agonist , glutamate receptor , cholinergic , nicotinic antagonist , chemistry , nmda receptor , dopamine , pharmacology , neuroscience , endocrinology , medicine , biology , receptor , biochemistry
We investigated the influence of nicotine on the release of ACh from rat striatal slices in the presence of domperidone to remove dopamine inhibition of ACh release. In medium facilitating glutamatergic transmission (with glycine and without Mg) nicotine increased the release of ACh evoked by mild potassium depolarization. This effect of nicotine was not present in resting conditions or when the tissue was fully depolarized. Enhancement of the release of ACh was prevented by tetrodotoxine, nicotinic antagonist mecamylamine, and glutamate NMDA antagonist MK 801. Our results suggest that nicotine increases ACh release indirectly by stimulation of nicotinic receptors on glutamatergic nerve terminals leading to the enhancement of glutamate release. Released glutamate in turn increases firing of cholinergic interneurons and ACh release. Nicotinic receptors on striatal glutamatergic nerve terminals perhaps play a role in the mechanism of striatal cholinergic hyperactivity observed in Parkinson's disease. Acknowledgements: Supported by grants GACR 305/01/0283 and GAAV 5011206.