Hypophysial GABA after ether stress, dexamethasone or inhibition of GABA catabolism.
Ether stress (2 X 2 min within 15 min) and dexamethasone treatment (1 mg/kg IP; 1, 3 and 12 hours before sacrifice), the procedures supposed to increase the activity of glutamate decarboxylase (GAD) in the hypothalamus, fail to affect the concentration of GABA in the rat hypophysis. Five and/or ten minutes post-mortem an increased GABA level in the hypothalamus and cingulate cortex, and a decreased GABA concentration in the hypophysis was found. Three and four hours after the IP administration of 1-cycloserine (50 mg/kg) and 1-glutamic acid-gamma-hydrazide (160 mg/kg) respectively (both drugs are inhibitors of GABA catabolism) the concentration of GABA raised in all the regions examined. On the basis of studies in the whole gland it might be concluded that the concentration of GABA in the hypophysis depends more on GABA release from extrahypophysial tissue and GABA degradation in the hypophysis than on the extrahypophysial GABA synthesis. Also on the basis of post-mortem studies in the whole gland no indication for the appearance of GABA synthesis in hypophysis could be found.
D000818:Animals; D003523:Cycloserine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology*; D004986:Ether / Q000494:pharmacology*; D005019:Ethyl Ethers / Q000494:pharmacology*; D018756:GABA Antagonists; D005971:Glutamates / Q000494:pharmacology; D006179:Gyrus Cinguli / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D008297:Male; D010902:Pituitary Gland / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013315:Stress, Psychological / Q000378:metabolism*; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005019:Ethyl Ethers; D018756:GABA Antagonists; D005971:Glutamates; D004986:Ether; C001296:L-glutamic acid-gamma-hydrazide; D005680:gamma-Aminobutyric Acid; D003907:Dexamethasone; D003523:Cycloserine