Possible role of gamma-aminobutyric acid synthesis in the mechanism of dexamethasone feedback action.
Specific inhibition of glutamic acid decarboxylase (GAD, EC 4.1.1.15; the main enzyme involved in the synthesis of gamma-aminobutyric acid) by mercaptopropionic acid interferes with the effect of dexamethasone on both the resting and stress-induced secretion of ACTH. It is postulated that dexamethasone may, at least in part, inhibit the secretion of ACTH via the induction of GAD, thereby raising the level of gamma-aminobutyric acid in the central nervous system.
D015097:3-Mercaptopropionic Acid / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000613:Aminobutyrates / Q000096:biosynthesis*; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D005246:Feedback; D005968:Glutamate Decarboxylase / Q000037:antagonists & inhibitors; D008297:Male; D051381:Rats; D013312:Stress, Physiological / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000096:biosynthesis*
D000613:Aminobutyrates; D005680:gamma-Aminobutyric Acid; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D015097:3-Mercaptopropionic Acid; D005968:Glutamate Decarboxylase; D003345:Corticosterone