抗惊厥药
引火模型
药理学
癫痫
火种
惊厥
神经炎症
癫痫发生
抽搐的
小胶质细胞
促炎细胞因子
医学
化学
内科学
炎症
神经科学
心理学
受体
作者
Mohammad Sayyah,Siamak Beheshti,Mohammad Ali Shokrgozar,Ali Eslamifar,Z. Deljoo,Alireza Khabiri,Ali Haeri Rohani
标识
DOI:10.1016/j.expneurol.2004.08.032
摘要
Ischaemic, excitotoxic and traumatic brain injuries have been associated with the occurrence of epileptic seizures. Microglia, the principal immune cells in the brain, produce a variety of proinflammatory and cytotoxic factors especially interleukin-1 (IL-1) early after an acute insult. We studied the effect of intracerebroventricularly administered IL-1beta on seizure acquisition and on fully kindled seizures in amygdala kindling model of epilepsy. IL-1beta (0.01 ng/rat) retarded acquisition of kindled behavioral seizures and growth of afterdischarges (AD). IL-1beta (0.01-10 ng/rat) also exhibited significant anticonvulsant effect on established kindled seizures and AD duration. This effect began 0.5 h after administration and was continued up to 72 h. Pretreatment of the kindled animals with nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester, or cyclooxygenase inhibitor, piroxicam, reversed the anticonvulsant effect of IL-1beta at early time points. Although most of the previous studies indicate a proconvulsant or convulsant property of IL-1, our results support a protective and antiepileptogenic role of IL-1beta.
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