Abstract
Following intraperitoneal injection to the rat, 90 to 95% of the administered radioactivity of γ-aminobutyric acid-1-C14 is eliminated as respiratory carbon dioxide during the subsequent 18-hour period. Urinary excretion of radioactivity during this period accounts for an additional 3 to 8% of the dose.
Simultaneous administration of hydrazine, semicarbazide, or isonicotinic acid hydrazide depressed metabolism of γ-aminobutyric acid-1-C14 to carbon dioxide. Concomitant significant increase in urinary radioactivity was observed only in the case of hydrazine. Administration of L-thyroxine to the rat daily for a period of 7 days prior to administration of γ-aminobutyric acid resulted in a decreased metabolism of γ-aminobutyric acid to carbon dioxide.
All of the foregoing compounds which inhibited conversion of γ-aminobutyric acid to carbon dioxide in vivo inhibited conversion of γ-aminobutyric acid to succinic semialdehyde by γ- aminobutyric-α-ketoglutaric transaminase activity of brain homogenates.
Footnotes
- Received March 16, 1961.
- © 1961, by The Williams & Wilkins Company
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