Tacke U, Braestrup C
Acta Pharmacol Toxicol (Copenh). 1984 Sep;55(3):252-9. doi: 10.1111/j.1600-0773.1984.tb02046.x.
Benzodiazepine receptors were investigated in the cerebral cortex, the hippocampus, the brainstem, and the cerebellum of audiogenic seizure (AGS)-susceptible and seizure-resistant (ER) control rats. In AGS-susceptible rats of Sprague-Dawley descent, muscimol (10-6 M and 3 x 10-5 M) activated the binding of 3H-diazepam (0.4 nM) significantly less than in ER-rats. This finding may be strain selective, since it was not observed in AGS-susceptible rats of Wistar descent. Specific binding of the convulsant benzodiazepine receptor ligand methyl 6,7-dimethoxy-4-ethyl carboline-3-carboxylate (3H-DMCM), the benzodiazepine receptor ligand 3H-diazepam and the chloride channel directed cage convulsant t-butylbicyclophosphorothionate 35S-TBPS were not significantly changed in AGS-susceptible as compared to control rats. Our findings indicate that a disturbance at the level of the benzodiazepine receptor/GABA receptor/chloride channel complex is not a likely general aetiological factor for audigenic seizures in rats.
在听源性癫痫（AGS）易感和抗癫痫（ER）对照大鼠的大脑皮层、海马体、脑干和小脑中研究了苯二氮䓬受体。在斯普拉格-道利品系的AGS易感大鼠中，蝇蕈醇（10-6 M和3×10-5 M）激活3H-地西泮（0.4 nM）结合的能力明显低于ER大鼠。这一发现可能具有品系选择性，因为在Wistar品系的AGS易感大鼠中未观察到这一现象。与对照大鼠相比，惊厥性苯二氮䓬受体配体6,7-二甲氧基-4-乙基咔啉-3-羧酸甲酯（3H-DMCM）、苯二氮䓬受体配体3H-地西泮以及氯离子通道导向性笼形惊厥剂硫代磷酸双环叔丁酯（35S-TBPS）的特异性结合在AGS易感大鼠中没有显著变化。我们的研究结果表明，苯二氮䓬受体/GABA受体/氯离子通道复合物水平的紊乱不太可能是大鼠听源性癫痫的普遍病因。
