慢性化学应激后γ-氨基丁酸能功能的变化。

Changes in GABAergic function after chronic chemical stress.

Acosta G B, Otero Losada M E, Rubio M C

Instituto de Investigaciones Farmacológicas, (ININFA), Consejo Nacional de Investigaciones Cientificas y Técnicas (CONICET), Buenos Aires, Argentina.

Gen Pharmacol. 1992 Mar;23(2):241-4. doi: 10.1016/0306-3623(92)90018-f.

Abstract

The function of the gamma-aminobutyric acid (GABA)-ergic system in certain areas of the rat brain was investigated after chronic chemical stress (exposure to either vapours 30 sec/day for 20 days). 2. GABA concentration, [3h] -GABA uptake and the activity of the synthesis enzyme glutamate decarboxylase (GAD) were measured. 3. Chronic stress: (a) reduced neuronal uptake of [3H] -GABA in the frontal cerebral cortex (43%) and increased non-neuronal uptake of [3H] -GABA in the hypothalamus (62%); (b) enhanced the activity of GAD (under subsaturating substrate concentration) in the frontal cortex (91%) and in the corpus striatum (69%); (c) did not modify GABA endogenous concentration; (d) did not affect the animals' body weight increase or produce any signs of toxicity. 4. The stimulation of GAD and reduction of [3H] -GABA neuronal uptake in the frontal cortex might suggest the stimulation of GABAergic neurotransmission induced by chronic stress in this area of the rat brain. Together with previous findings the frontal cortex would appear to be a key area in chronic stress processing.

摘要

在慢性化学应激（每天暴露于蒸汽30秒，持续20天）后，研究了大鼠脑某些区域中γ-氨基丁酸（GABA）能系统的功能。2. 测量了GABA浓度、[3H]-GABA摄取以及合成酶谷氨酸脱羧酶（GAD）的活性。3. 慢性应激：（a）降低了额叶皮质中[3H]-GABA的神经元摄取（43%），并增加了下丘脑非神经元对[3H]-GABA的摄取（62%）；（b）增强了额叶皮质（91%）和纹状体（69%）中GAD的活性（在底物浓度不饱和的情况下）；（c）未改变GABA内源性浓度；（d）未影响动物体重增加，也未产生任何毒性迹象。4. 额叶皮质中GAD的刺激和[3H]-GABA神经元摄取的减少可能表明慢性应激在大鼠脑该区域诱导了GABA能神经传递的刺激。与先前的研究结果一起，额叶皮质似乎是慢性应激处理的关键区域。