Abstract
Chronic treatment of mice with the specific gamma-aminobutyric acid(B) (GABA(B)) receptor antagonist (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50,911) increased both the number of GABA(B) receptors in the whole brain (measured as [3H]CGP 54626 [S-(R,R)]-3-[[1-(3,4-dichlorophenyl)amino]-2-hydroxypropyl](cyclohexylmethyl)phosphinic acid hydrochloride binding) and the ability of baclofen to activate GABA(B) receptor coupled G-protein (measured as % reduction of the EC50 of baclofen to activate [35S]GTP(gamma)S binding). The results indicate that persistent blockade of GABA(B) receptors leads to their compensatory up-regulation and suggest that GABA(B) receptors are tonically activated by endogenous GABA.
MeSH terms
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Animals
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Baclofen / pharmacology
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Binding, Competitive / drug effects
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Brain / drug effects
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Brain / metabolism
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Dose-Response Relationship, Drug
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GABA Agonists / pharmacology
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GABA-B Receptor Agonists
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GABA-B Receptor Antagonists
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Guanosine 5'-O-(3-Thiotriphosphate) / metabolism
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Male
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Mice
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Mice, Inbred DBA
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Morpholines / pharmacology*
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Organophosphorus Compounds / metabolism
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Receptors, GABA-B / metabolism*
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Sulfur Radioisotopes
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Tritium
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Up-Regulation
Substances
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(+)-(S)-5,5-dimethylmorpholinyl-2-acetic acid
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GABA Agonists
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GABA-B Receptor Agonists
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GABA-B Receptor Antagonists
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Morpholines
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Organophosphorus Compounds
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Receptors, GABA-B
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Sulfur Radioisotopes
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Tritium
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CGP 54626
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Guanosine 5'-O-(3-Thiotriphosphate)
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Baclofen