Hypothalamic GABA system and plasma corticosterone in ether stressed rats.
Exposure of rats to the ether stress (2 X 2 min within 15 min) activated the hypothalamo-hypophyseal-adrenal (HHA) axis, as evidenced by the increased plasma corticosterone concentration, and affected the hypothalamic GABA system. The aminooxyacetic acid (AOAA) or L-cycloserine-induced accumulation of GABA was decreased, and the activity of glutamate decarboxylase (GAD), the enzyme responsible for GABA synthesis, was increased following ether stress. The concentration of GABA and the activity of GABA: 2-oxoglutarate aminotransferase (GABA-T), the enzyme responsible for GABA catabolism, remained unchanged under given conditions. Diazepam, a drug known to potentiate GABA-ergic transmission, elevated the concentration of plasma corticosterone, but prevented its further increase by ether stress. In spite of the diminished accumulation of GABA, the results might suggest that ether stress activates the hypothalamic GABA system, which is then able to prevent a further response of the HHA axis to stress.
D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000097:blood*; D003523:Cycloserine / Q000494:pharmacology; D003975:Diazepam / Q000494:pharmacology; D004986:Ether / Q000633:toxicity*; D005019:Ethyl Ethers / Q000633:toxicity*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology*; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013312:Stress, Physiological / Q000503:physiopathology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005019:Ethyl Ethers; D004986:Ether; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D003523:Cycloserine; D005968:Glutamate Decarboxylase; D003975:Diazepam; D003345:Corticosterone