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GABAergic Modulation of Striatal Cholinergic Interneurons: An In Vivo Microdialysis Study
Author(s) -
DeBoer P.,
Westerink B. H. C.
Publication year - 1994
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.1471-4159.1994.62010070.x
Subject(s) - muscimol , bicuculline , gabaa receptor , gabaergic , cholinergic , agonist , acetylcholine , gaba receptor antagonist , baclofen , chemistry , gaba receptor , microdialysis , gamma aminobutyric acid , medicine , endocrinology , receptor , pharmacology , biology , central nervous system , biochemistry
Abstract: Striatal cholinergic interneurons have been shown to receive input from Striatal γ‐aminobutyric acid (GABA)‐containing cell elements. GABA is known to act on two different types of receptors, the GABA A and the GABA 6 receptor. Using in vivo microdialysis, we have studied the effect of intrastriatal application of the GABA A ‐selective compounds muscimol and bicuculline and the GA‐ BA B ‐selective compounds baclofen and 2‐hydroxysaclofen, agonists and antagonists, respectively, at GABA receptors, on the output of Striatal acetylcholine (ACh). Intrastriatal infusion of 1 and 10 μmol/L concentrations of the GABA A antagonist bicuculline resulted in a significant increase in Striatal ACh output, whereas infusion of 1 and 10 /μmol/L concentrations of the GABA A agonist muscimol significantly decreased the output of Striatal ACh. Both compounds were ineffective in changing the output of Striatal ACh at lower concentrations. Infusion of concentrations up to 100 μmol/L of the GABA B ‐selective antagonist 2‐hydroxy‐saclofen failed to affect Striatal ACh output, whereas infusion of 10 and 100 μmol/L baclofen, but not 0.1 and 1 μmol/L baclofen, significantly decreased the output of Striatal ACh. Thus, agonist‐stimulation of GABAA and GABA B receptors decreases the output of striatal ACh in a dose‐dependent fashion, whereas the GABAergic system appears to inhibit tonically the output of striatal ACh via GABA A receptors, but not via GABA B receptors. We hypothesize that although GABA A mediated regulation of striatal ACh occurs via GABA receptors on the cholinergic neuron, the GABA B mediated effects may be explained by presynaptic inhibition of the glutamatergic input of the striatal cholinergic neuron.