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Optogenetic control of thalamus as a tool for interrupting penicillin induced seizures

机译:丘脑的致敏控制作为中断青霉素诱导癫痫发作的工具

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Penicillin epilepsy model, whose discharge resembles that of human absence epilepsy, is one of the most useful acute experimental epilepsy models. Though closed-loop optogenetic strategy of interrupting seizures was proved sufficient to switch off epilepsy by controlling thalamus in the post-lesion partial chronic epilepsy model, doubts still exist in absence epilepsy attenuation through silencing thalamus. Here we directly arrested the thalamus to modulate penicillin-induced absence seizures through pseudorandom responsive stimulation on eNpHR-transfected rats. Our data suggested that the duration of epileptiform bursts under light conditions, compared with no light conditions, did not increase or decrease when modulated specific eNpHR-expressing neurons in thalamus.
机译:青霉素癫痫模型,其放电类似于人类缺失癫痫,是最有用的急性实验性癫痫模型之一。尽管证明,通过控制秋季部分慢性癫痫模型的丘脑,证明了闭环癫痫发作的闭路策略足以关闭癫痫,仍然存在于通过沉默的丘脑缺乏癫痫衰减而存在疑惑。在这里,我们直接捕获丘脑以调节青霉素诱导的缺失癫痫发作,通过对浓缩的大鼠的盲肠响应刺激来调节缺乏癫痫发作。我们的数据表明,在轻质条件下癫痫脉冲脉冲的持续时间与无光线条件相比,在丘脑中调节特异性苯染力的神经元没有增加或降低。

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