Smith K L, Swann J W
Brain Res. 1987 Jan 6;400(2):371-6. doi: 10.1016/0006-8993(87)90637-8.
Bath application of therapeutic concentrations of the anticonvulsant carbamazepine suppressed penicillin-induced synchronized afterdischarging in immature rat CA3 hippocampal pyramidal cells. Afterdischarging was completely abolished in all preparations at a concentration of 30 microM (IC50 = 8.5 +/- 1.4 microM; mean +/- S.E.M.). The duration of the preceding epileptiform burst was not altered at this concentration and was diminished by only 24.4 +/- 1.2% at a supratherapeutic concentration of 100 microM. These results suggest that a carbamazepine-sensitive neurophysiological mechanism distinct from those responsible for epileptiform burst generation plays a key role in the generation of afterdischarges in developing hippocampus.
在未成熟大鼠CA3海马锥体细胞中,应用治疗浓度的抗惊厥药卡马西平进行脑池给药可抑制青霉素诱导的同步放电后发放。在浓度为30微摩尔时,所有制剂中的放电后发放均完全消除(IC50 = 8.5 +/- 1.4微摩尔;平均值 +/- 标准误)。在此浓度下,先前癫痫样爆发的持续时间未改变,而在超治疗浓度100微摩尔时仅减少了24.4 +/- 1.2%。这些结果表明,一种对卡马西平敏感的神经生理机制不同于那些负责癫痫样爆发产生的机制,在发育中的海马体放电后发放的产生中起关键作用。