琥珀酸对大鼠化学性点燃和杏仁核电刺激性点燃的抑制作用

目的:研究琥珀酸对大鼠戊四哇化学性点燃(kindling)发作及杏仁核电刺激点燃发作的影响及作用机制.方法:建立大鼠戊四唑化学性点燃模型和杏仁核电刺激点燃癫痫模型,测定琥珀酸对点燃发作的脑电活动及行为变化指标的影响.测定琥珀酸对GABA_A受体拮抗剂印防己毒素诱发小鼠惊厥的影响.结果:琥珀酸(100-400 mg/kg,iP)对两种点燃模型有显著抑制作用,降低发作强度和全身性发作百分率(P<0.05,P<0.01),可升高杏仁核电刺激点燃大鼠的局灶性后放电阈值(P<0.05,P<0.01),以上反应呈剂量效应关系。琥珀酸可延长印防己毒素诱发小鼠惊厥的潜伏期(P<0.05,P<0.01).结论:琥珀酸对大鼠戊四唑化学性点燃和脑杏仁核电刺激点燃发作有抑制作用,其机制可能与增强GABA_A受体功能有关.

Inhibitory effects of succinic acid on chemical kindling and amygdala electrical kindling in rats

AIM: To investigate the effects and mechanism of succinic acid on pentylenetetrazol (PTZ) chemical kindling and amygdala electrical kindling in rats. METHODS: PTZ chemical kindling and amygdala electrical kindling models were established in rats. The effects of succinic acid on the behavior and afterdischarge of kindled rats were observed. The mice were pretreated with succinic acid, 30 min later, picrotoxin, a GABAA receptor antagonist was given by ip, then the effects of succinic acid on mice were observed. RESULTS: Succinic acid (100-400 mg/kg, ip) dose-dependently inhibited PTZ chemical and amygdala kindled seizure (P<0.05, P<0.01), elevated the afterdis-charge threshold, and reduced the Racine's stage of amygdala kindling rats (P<0.05, P<0.01); succinic acid (200-400 mg/kg, ip) inhibited picrotoxin-convulsion in mice (P<0.05, P<0.01). CONCLUSION: Succinc acid inhibits PTZ chemical and amygdala electrical kindling in rats, and the inhibition mechanism may be related to the enhance-ment of GABAergic system action in the brain, especially through GABAA receptors.