Manev H, Pericić D
Pharmacol Biochem Behav. 1983 Jun;18(6):847-50. doi: 10.1016/s0091-3057(83)80003-3.
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.
将大鼠暴露于乙醚应激（15分钟内2次，每次2分钟）会激活下丘脑 - 垂体 - 肾上腺（HHA）轴，血浆皮质酮浓度升高证明了这一点，并且会影响下丘脑的GABA系统。氨基氧乙酸（AOAA）或L - 环丝氨酸诱导的GABA积累减少，而负责GABA合成的谷氨酸脱羧酶（GAD）的活性在乙醚应激后增加。在给定条件下，GABA的浓度以及负责GABA分解代谢的GABA：2 - 氧代戊二酸氨基转移酶（GABA - T）的活性保持不变。地西泮是一种已知能增强GABA能传递的药物，它会提高血浆皮质酮浓度，但能阻止其因乙醚应激而进一步升高。尽管GABA的积累减少，但结果可能表明乙醚应激激活了下丘脑的GABA系统，进而能够阻止HHA轴对压力的进一步反应。
