Hillmann M, Wilce P A, Shanley B C
Alcohol Research Unit, Department of Biochemistry, University of Queensland, St Lucia, Queensland 4067, Australia.
Neurochem Int. 1988;13(1):69-73. doi: 10.1016/0197-0186(88)90104-0.
Chronic treatment of male Wistar rats with ethanol by inhalation did not affect the binding of [(3)H]flunitrazepam, [(3)H]GABA or [(3)H]muscimol to extensively washed synaptic membranes. Neither the affinity (K(d)) nor the number of binding sites (Bmax) for these ligands was changed. However, GABA enhancement of [(3)H]flunitrazepam binding was significantly decreased by approx. 40% in ethanol-treated animals (172% compared to 215%). Acute treatment with ethanol did not produce changes in the binding of [(3)H]flunitrazepam or [(3)H]muscimol. These findings suggest that chronic ethanol treatment leads to uncoupling of the various receptor sites on the GABA-benzodiazepine receptor ionophore-complex in the brain.
通过吸入方式对雄性Wistar大鼠进行慢性乙醇处理，并未影响[(3)H]氟硝西泮、[(3)H]γ-氨基丁酸（GABA）或[(3)H]蝇蕈醇与充分洗涤后的突触膜的结合。这些配体的亲和力（K(d)）和结合位点数量（Bmax）均未改变。然而，在乙醇处理的动物中，GABA对[(3)H]氟硝西泮结合的增强作用显著降低了约40%（与215%相比为172%）。乙醇急性处理并未使[(3)H]氟硝西泮或[(3)H]蝇蕈醇的结合产生变化。这些发现表明，慢性乙醇处理会导致大脑中GABA-苯二氮䓬受体离子通道复合物上的各种受体位点解偶联。
