RT Journal Article
SR Electronic
T1 FACTORS CONTROLLING THE METABOLISM OF γ-AMINOBUTYRIC ACID
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 222
OP 226
VO 134
IS 2
A1 HORVATH, ANTONIO
A1 ORREGO, FERNANDO
A1 McKENNIS, HERBERT
YR 1961
UL http://jpet.aspetjournals.org/content/134/2/222.abstract
AB 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. © 1961, by The Williams & Wilkins Company