Neuroethologically delineated differences in the seizure behavior of Synapsin 1 and Synapsin 2 knock-out mice
Neuroethologically delineated differences in the seizure behavior of Synapsin 1 and Synapsin 2 knock-out mice
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DOI：
10.1016/j.eplepsyres.2011.12.004
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发表时间：
2012-05-01
影响因子：
2.2
通讯作者：
Heggelund, Paul
中科院分区：
文献类型：
--
作者：
Etholm, Lars;Bahonjic, Elma;Heggelund, Paul
高度同源的神经末端磷蛋白突触蛋白I和突触蛋白II已经通过突触蛋白基因突变与人类癫痫疾病之间的关联与癫痫的发病机制相关联，并且与在遗传上耗尽这些蛋白中的一种或两种的小鼠中处理诱导的癫痫发作的观察相关联。虽然缺乏突触蛋白I和突触蛋白II的小鼠的癫痫发作行为得到了很好的表征，但缺乏突触蛋白I和突触蛋白II的小鼠的癫痫发作行为却没有得到很好的研究。通过对4个半月龄的Synapsin 1和2基因敲除小鼠（Syn1KO和Syn2KO小鼠）完全建立的癫痫发作行为进行所谓的基于神经行为学的分析，本研究揭示了两种基因型小鼠癫痫发作行为的显著差异：而Syn1KO小鼠显示部分和全身性前脑癫痫发作活动，Syn2KO小鼠仅显示完全全身性前脑癫痫发作。早期癫痫发作行为分析表明，Syn2KO小鼠的成熟癫痫发作模式从相似至2月龄迅速建立，此时Syn1KO部分性癫痫发作罕见，并且几乎不存在Syn1KO全身性癫痫发作。这两个品系特异性的行为表型表明，这些高度相关的蛋白质在结构、功能和表达上的细微差异可能是癫痫发作产生神经活动的重要因素。(C)2011 Elsevier B.V.保留所有权利。
The highly homologous nerve terminal phosphoproteins synapsin I and synapsin II have been linked to the pathogenesis of epilepsy through associations between synapsin gene mutations and epileptic disease in humans and to the observation of handling induced seizures in mice genetically depleted of one or both of these proteins. Whereas seizure behavior in mice lacking both synapsin I and synapsin II is well characterized, the seizure behavior in mice lacking either is less well studied. Through so called neuroethologically based analyses of fully established seizure behavior in Synapsin 1 and 2 knock-out mice (Syn1KO and Syn2KO mice) aged 4 1/2 months, this study reveals significant differences in the seizure behavior of the two genotypes: whereas Syn1KO mice show both partial and generalized forebrain seizure activity, Syn2KO mice show only fully generalized forebrain seizures. Analysis of seizure behavior at earlier stages shows that the mature seizure pattern in Syn2KO mice establishes rapidly from the age of similar to 2 months, when Syn1KO partial seizures are rare, and Syn1KO generalized seizures are almost absent. The specific behavioral phenotypes of the two strains suggest that the slight differences in structure, function and expression of these highly related proteins could be important factors during seizure generating neural activity. (C) 2011 Elsevier B.V. All rights reserved.