Miller J A, Richter J A
Br J Pharmacol. 1985 Jan;84(1):19-25.
The effects of several anticonvulsant drugs on sodium-dependent high affinity choline uptake (HACU) in mouse hippocampal synaptosomes was investigated. HACU was measured in vitro after in vivo administration of the drug to mice. HACU was inhibited by drugs which have in common the ability to facilitate gamma-aminobutyric acid (GABA) transmission, pentobarbitone, phenobarbitone, barbitone, diazepam, chloridiazepoxide, and valproic acid. Dose-response relationships were determined for these drugs and the drugs' potencies at inhibiting HACU correlated well with their anticonvulsant potencies. Clonazepam, ethosuximide, carbamazepine, and barbituric acid had no effect on HACU in the doses used while phenytoin and trimethadione stimulated HACU. These results suggest that certain anticonvulsants may elicit a part of their anticonvulsant activity by modulating cholinergic neurones. This effect may be mediated through a GABA mechanism.
研究了几种抗惊厥药物对小鼠海马突触体中钠依赖性高亲和力胆碱摄取（HACU）的影响。在给小鼠体内给药后，体外测量HACU。具有促进γ-氨基丁酸（GABA）传递能力的药物，如戊巴比妥、苯巴比妥、巴比妥、地西泮、氯氮卓和丙戊酸，均可抑制HACU。确定了这些药物的剂量-反应关系，并且这些药物抑制HACU的效力与其抗惊厥效力密切相关。在所用剂量下，氯硝西泮、乙琥胺、卡马西平和巴比妥酸对HACU无影响，而苯妥英和三甲双酮则刺激HACU。这些结果表明，某些抗惊厥药物可能通过调节胆碱能神经元来发挥其部分抗惊厥活性。这种作用可能是通过GABA机制介导的。
