Racine R, Livingston K, Joaquin A
Electroencephalogr Clin Neurophysiol. 1975 Apr;38(4):355-65. doi: 10.1016/0013-4694(75)90260-6.
Procaine HCl and diphenylhydantoin (DPH) increased the duration and propagation of epileptiform afterdischarges (ADs) produced by electrical stimulation of the amygdala in rats. Procaine and DPH also increased the rate of seizure development (kindling) produced by repeated stimulation of the amygdala. Procaine and to a limited extentDPH would themselves act as convulsants in well kindled subjects. Diazepam, on the other hand, retarded or blocked amygdaloid kindling. Diazepam trigered a high frequency (20-30 c/sec) rhtthm in the amygdala, hippocampus and preoptic area. None of these drugs had any significant effect on potentials evoked in secondary limbic sites by single electrical pulses applied to the amygdala. Also, none of these drugs had any effect on recruiting or post-tetanic potentiation (PTP) in secondary sites produced by amygdala stimulation and none of the drugs had any effect on amygdaloid AD thresholds. The effects of these drugs on the responses evoked by anterior neocortex stimulation were quite different. Diazepam had no effect on any of the characteristics of the discharge or convulsion even at twice the dose levels used for the amygdala group. Procaine and DPH, however, blocked not only the eonvulsion but the AD as well. Eighty percent of the procaine- and DPH-treated rats failed to respond with neocortical AD even at current levels as high as 2000 muA. The few cortically stimulated subjects that did respond with an AD showed a subcortical rather than a neocortical seizure response. DPH had no effect on recruiting or PTP of the transcallosal response. Both procaine and DPH produced a weak but significant increase in the amplitude of the transcallosal evoked potential, while diazepam produce a weak decrement in that response.
盐酸普鲁卡因和苯妥英（DPH）可延长电刺激大鼠杏仁核所产生的癫痫样后放电（ADs）的持续时间并促进其传播。普鲁卡因和DPH还可加快重复刺激杏仁核所产生的癫痫发作发展（点燃）速度。在充分点燃的实验对象中，普鲁卡因以及在一定程度上的DPH自身会起到惊厥剂的作用。另一方面，地西泮会延缓或阻断杏仁核点燃。地西泮在杏仁核、海马体和视前区引发高频（20 - 30次/秒）节律。这些药物对施加于杏仁核的单个电脉冲在次级边缘部位所诱发的电位均无显著影响。此外，这些药物对杏仁核刺激在次级部位所产生的募集反应或强直后增强（PTP）均无影响，且对杏仁核AD阈值也无影响。这些药物对前脑新皮质刺激所诱发反应的影响则大不相同。即使给予的剂量是用于杏仁核组的两倍，地西泮对放电或惊厥的任何特征均无影响。然而，普鲁卡因和DPH不仅阻断惊厥，还阻断AD。接受普鲁卡因和DPH治疗的大鼠中，80%即使在电流高达2000微安时也未出现新皮质AD反应。少数经皮质刺激且出现AD反应的实验对象表现出的是皮质下而非新皮质癫痫发作反应。DPH对胼胝体反应的募集或PTP无影响。普鲁卡因和DPH均使胼胝体诱发电位的幅度出现微弱但显著的增加，而地西泮则使该反应出现微弱的降低。
