Morag M, Myslobodsky M
Life Sci. 1982 May 10;30(19):1671-7. doi: 10.1016/0024-3205(82)90500-8.
A hypothesis was considered that anti-epileptic potency of sodium valproate (VPA) may be associated with its action via the benzodiazepine system. The ability of anti-petit mal drugs to suppress the slow secondary negative wave (SNW) of the visually evoked potential was used as a sensitive electrophysiological "tag" for comparison of VPA (200 mg/kg, i.p.) and Diazepam (5 mg/kg, i.p.) effects. Both drugs induced a profound inhibition of the SNW. Benzodiazepine antagonists Ro 5-3663 (2 mg/kg, i.p.) and Ro 15-1788 (5 mg/kg, i.p.) caused recovery of the SNW amplitude within several minutes of injection. Both antagonists abolished immobility and sedation produced by VPA and Diazepam. The possibility should be considered that therapeutic effects of VPA are mediated through the benzodiazepine receptor coupled to GABA.
有人提出一种假说，即丙戊酸钠（VPA）的抗癫痫效力可能与其通过苯二氮䓬系统的作用有关。将抗失神发作药物抑制视觉诱发电位慢继发性负波（SNW）的能力用作一种敏感的电生理“标记”，以比较VPA（200mg/kg，腹腔注射）和地西泮（5mg/kg，腹腔注射）的效果。两种药物均对SNW产生了显著抑制。苯二氮䓬拮抗剂Ro 5-3663（2mg/kg，腹腔注射）和Ro 15-1788（5mg/kg，腹腔注射）在注射后几分钟内使SNW振幅恢复。两种拮抗剂均消除了VPA和地西泮产生的不动和镇静作用。应考虑VPA的治疗作用是通过与GABA偶联的苯二氮䓬受体介导的可能性。
