Takada R, Saito K, Matsuura H, Inoki R
Department of Pharmacology, Osaka University, Faculty of Dentistry, Suita, Japan.
Alcohol. 1989 Mar-Apr;6(2):115-9. doi: 10.1016/0741-8329(89)90035-9.
The effect of ethanol on GABA receptors was studied in hippocampal slices and membrane preparations of the rat brain. In slice preparation, ethanol enhanced the GABA inhibition of the population spikes evoked in CA 1 pyramidal cells by Schaffer collateral stimulation. The effect of ethanol was dose-dependent being observed with minimal concentration of 70 mM. In 3H-GABA binding experiments, ethanol enhanced the binding to fresh membranes with no change in the affinity. Maximal stimulation was observed at ethanol concentration of 70 mM. In hippocampal slices or membrane preparations obtained from ethanol- or barbital-administered rats chronically, ethanol failed to enhance GABA function. Thus, the present study demonstrated the involvement of GABA in central effect of ethanol. Also suggested in GABA was the involvement in the development of cross-tolerance between ethanol and barbiturates.
在大鼠脑海马切片和膜制剂中研究了乙醇对γ-氨基丁酸(GABA)受体的影响。在切片制备中,乙醇增强了通过Schaffer侧支刺激在CA1锥体细胞中诱发的群体峰电位的GABA抑制作用。乙醇的作用呈剂量依赖性,在最低浓度70 mM时即可观察到。在3H-GABA结合实验中,乙醇增强了与新鲜膜的结合,亲和力无变化。在乙醇浓度为70 mM时观察到最大刺激。在长期给予乙醇或巴比妥酸盐的大鼠获得的海马切片或膜制剂中,乙醇未能增强GABA功能。因此,本研究证明了GABA参与乙醇的中枢效应。GABA还提示参与了乙醇和巴比妥酸盐之间交叉耐受性的发展。