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Effects of Increased γ‐Aminobutyric Acid Levels on GAD 67 Protein and mRNA Levels in Rat Cerebral Cortex
Author(s) -
Rimvall Karin,
Sheikh Sabi.,
Martin David L.
Publication year - 1993
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 - 10.1111/j.1471-4159.1993.tb03206.x
Subject(s) - glutamate decarboxylase , aminobutyric acid , messenger rna , endocrinology , medicine , cerebral cortex , glutamate receptor , gabaergic , gamma aminobutyric acid , chemistry , glutamic acid , enzyme , biology , amino acid , biochemistry , receptor , gene , inhibitory postsynaptic potential
Rats were injected with saline or the γ‐aminobutyric acid (GABA) transaminase inhibitor γ‐vinyl‐GABA for 7 days and the effects on GABA content and glutamic acid decarboxylase (GAD) activity, and the protein and mRNA levels of the two forms of GAD (GAD 67 and GAD 65 ) in the cerebral cortex were studied. γ‐Vinyl‐GABA induced a 2.3‐fold increase in GABA content, whereas total GAD activity decreased by 30%. Quantitative immunoblotting showed that the decline in GAD activity was attributable to a 75–80% decrease in GAD 67 levels, whereas the levels of GAD 65 remained unchanged. RNA slot‐blotting with a 32 P‐labeled GAD 67 cDNA probe demonstrated that the change in GAD 67 protein content was not associated with a change in GAD 67 mRNA levels. Our results suggest that GABA specifically controls the level of GAD 67 protein. This effect may be mediated by a decreased translation of the GAD 67 mRNA and/or a change in the stability of the GAD 67 protein.