Weissman B A, Bolger G T
Department of Pharmacology, Israel Institute for Biological Research, Ness Ziona.
Brain Res Bull. 1987 Dec;19(6):673-8. doi: 10.1016/0361-9230(87)90053-0.
The effects of chemically and electrically-evoked seizures on [3H]nitrendipine binding to voltage-dependent calcium channels in mouse brain were determined 30 and 60 min following the initiation of convulsions. While maximal electroconvulsive shock, pentylenetetrazol and strychnine exhibited either no or marginal effects, Ro 5-4864 produced a decrease (14%) in the Bmax of [3H]nitrendipine at 30 min but not 60 min. The convulsant dihydropyridine calcium channel activator, BAY K 8644, produced a significant increase in the Kd (31%) of [3H]nitrendipine at 30 min, and a significant increase in both the Bmax (21%) and Kd (28%) of [3H]nitrendipine 60 min following the initiation of convulsions. While maximal electroconvulsive shock, pentylenetetrazol and strychnine exhibited either no or marginal effects, Ro 5-4864 produced a decrease (14%) in the Bmax of [3H]nitrendipine at 30 min but not 60 min following the initiation of convulsions. These findings indicate that modulation of voltage-dependent calcium channels by certain convulsants may be important in the genesis of seizures or in post-ictal compensatory processes.
在惊厥发作开始后的30分钟和60分钟，测定了化学和电诱发惊厥对小鼠脑中[3H]尼群地平与电压依赖性钙通道结合的影响。虽然最大电休克、戊四氮和士的宁要么没有影响，要么只有轻微影响，但Ro 5-4864在30分钟时使[3H]尼群地平的Bmax降低了14%，而在60分钟时没有降低。惊厥性二氢吡啶钙通道激活剂BAY K 8644在惊厥发作开始后30分钟时使[3H]尼群地平的Kd显著增加（31%），在60分钟时使[3H]尼群地平的Bmax（21%）和Kd（28%）均显著增加。虽然最大电休克、戊四氮和士的宁要么没有影响，要么只有轻微影响，但Ro 5-4864在惊厥发作开始后30分钟时使[3H]尼群地平的Bmax降低了14%，而在60分钟时没有降低。这些发现表明，某些惊厥剂对电压依赖性钙通道的调节可能在癫痫发作的发生或发作后补偿过程中起重要作用。
