Bowyer J F, Albertson T E, Winters W D
Epilepsia. 1983 Jun;24(3):356-67. doi: 10.1111/j.1528-1157.1983.tb04899.x.
The effects of several excitant-convulsants, cataleptic anesthetics, and gamma-acetylenic gamma-aminobutyric acid (GABA) were tested on seizures kindled by repetitive electrical stimulation of the motor cortex in the rat. A dose response was determined for each drug. For most of the drugs, the doses tested ranged from those causing some signs of behavioral excitation to those inducing epileptoid activity. None of the excitant-convulsants, including strychnine, physostigmine, amphetamine, bicuculline, or pentylenetetrazol, increased the afterdischarge duration (AD) or behavioral response (BR) of the partially developed (PD-KCS) or generalized fully developed (KCS) kindled cortical seizures. Whereas pentylenetetrazol had no effect on the PD-KCS, it has been previously shown to increase significantly the AD and BR of the developing or partially developed amygdaloid kindled seizures. Lidocaine, gamma-butyrolactone, gamma-acetylenic GABA, phencyclidine, and ketamine inhibited the AD of the KCS by greater than or equal to 80%. Lidocaine, phencyclidine, and ketamine decreased whereas gamma-butyrolactone and gamma-acetylenic GABA increased the AD of the PD-KCS. The ability of gamma-butyrolactone and gamma-acetylenic GABA to potentiate the PD-KCS while inhibiting the KCS presents a paradox not readily explained. Our results combined with previous reports of the effects of gamma-butyrolactone and gamma-acetylenic GABA on amygdaloid kindled seizures indicate that the KCS is more susceptible to GABAnergic and cataleptic inhibition than is the fully developed amygdaloid kindled seizures. The differences between the response of cortical kindled and that of amygdaloid kindled seizures to some of the drugs tested may indicate differences in the physiological and biochemical mechanisms involved in producing these seizures.
在大鼠中，测试了几种兴奋性惊厥剂、强直性麻醉剂和γ-乙炔基γ-氨基丁酸（GABA）对通过重复电刺激运动皮层引发的癫痫发作的影响。确定了每种药物的剂量反应。对于大多数药物，测试剂量范围从引起一些行为兴奋迹象的剂量到诱发类癫痫样活动的剂量。包括士的宁、毒扁豆碱、苯丙胺、荷包牡丹碱或戊四氮在内的兴奋性惊厥剂均未增加部分发展型（PD-KCS）或全身性完全发展型（KCS）点燃性皮层癫痫发作的放电后持续时间（AD）或行为反应（BR）。虽然戊四氮对PD-KCS没有影响，但先前已表明它可显著增加正在发展或部分发展的杏仁核点燃性癫痫发作的AD和BR。利多卡因、γ-丁内酯、γ-乙炔基GABA、苯环利定和氯胺酮对KCS的AD抑制率大于或等于80%。利多卡因、苯环利定和氯胺酮降低了PD-KCS的AD，而γ-丁内酯和γ-乙炔基GABA增加了PD-KCS的AD。γ-丁内酯和γ-乙炔基GABA增强PD-KCS同时抑制KCS的能力呈现出一个难以轻易解释的矛盾现象。我们的结果与先前关于γ-丁内酯和γ-乙炔基GABA对杏仁核点燃性癫痫发作影响的报道相结合，表明KCS比完全发展的杏仁核点燃性癫痫发作更容易受到GABA能和强直性抑制的影响。皮层点燃性癫痫发作和杏仁核点燃性癫痫发作对某些测试药物反应的差异可能表明产生这些癫痫发作所涉及的生理和生化机制存在差异。
