Ticku M K
University of Texas Health Science Center, Department of Pharmacology, San Antonio 78284-7764.
Alcohol Alcohol Suppl. 1987;1:657-62.
Ethanol interacts allosterically with the picrotoxin binding sites on the oligomeric GABA receptor complex in vitro. Chronic ethanol treatment does not alter the binding properties of [35S]t-butyl-bicyclophosphorothioate or [3H]flunitrazepam to brain membranes. In behavioral studies, ethanol prevents convulsions induced by bicuculline, picrotoxin and maximal electroshock seizures. Further, subprotective dose of ethanol in combination with other facilitators of GABAergic transmission, provide protection against these convulsions. Finally, ethanol potentiates the effect of GABA on 36Cl-influx in cultured spinal cord neurons. These studies indicate a role for GABAAergic transmission in the actions of ethanol.
在体外，乙醇与寡聚GABA受体复合物上的印防己毒素结合位点发生变构相互作用。慢性乙醇处理不会改变[35S]叔丁基双环磷硫代酸酯或[3H]氟硝西泮与脑膜的结合特性。在行为学研究中，乙醇可预防荷包牡丹碱、印防己毒素和最大电休克惊厥诱导的惊厥。此外，亚保护剂量的乙醇与其他GABA能传递促进剂联合使用，可预防这些惊厥。最后，乙醇可增强GABA对培养脊髓神经元中36Cl内流的作用。这些研究表明GABAA能传递在乙醇作用中发挥作用。
