gamma-Aminobutyric acid (GABA) induces a receptor-mediated reduction in GABA(A) receptor alpha subunit messenger RNAs in embryonic chick neurons in culture

gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in brain, is known to interact with a subclass of receptors that activate a ligand-gated chloride ion channel. Exposure of cultured embryonic chick neurons to physiological concentrations of GABA results in a time-dependent down-r...

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Bibliographic Details
Published in:The Journal of biological chemistry 1991-04, Vol.266 (10)
Main Authors: Montpied, P. (National Institute of Mental Health, Bethesda, MD), Ginns, E.I, Martin, B.M, Roca, D, Farb, D.H, Paul, S.M
Format: Article
Language:English
Subjects:
ACIDE AMINE
AMINOACIDOS
ARN MENSAJERO
ARN MESSAGER
EMBRIONES ANIMALES
EMBRYON ANIMAL
GENETICA
GENETIQUE
NERF
NERVIOS
POLLITO
POUSSIN
TEJIDOS ANIMALES
TISSU ANIMAL
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Summary:gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in brain, is known to interact with a subclass of receptors that activate a ligand-gated chloride ion channel. Exposure of cultured embryonic chick neurons to physiological concentrations of GABA results in a time-dependent down-regulation of these GABA(A) receptors. To delineate the cellular mechanism(s) responsible for agonist-induced down-regulation of GABA(A) receptors we quantified the levels of GABA(A) receptor a subunit messenger RNAs, which encode the subunit(s) containing agonist recognition site(s), and observed a marked reduction in a subunit mRNAs following exposure of embryonic chick neurons to GABA. Both the down-regulation of GABA(A) receptors and the reduction in a subunit mRNAs induced by GABA were completely antagonized by the specific GABA(A) receptor antagonist SR-95531. These data demonstrate the presence of an agonist-induced receptor-mediated mechanism for regulating the expression of receptor subunit-encoding mRNAs that may be involved in the development of tolerance to the pharmacological actions of drugs known to act via GABA(A) receptors
ISSN:0021-9258
1083-351X