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The rearrangement of filamentous actin in mossy fiber synapses in pentylenetetrazol-kindled C57BL/6 mice

机译:戊四氮点燃的C57BL / 6小鼠苔藓纤维突触中丝状肌动蛋白的重排

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摘要

Chemical kindling, as an experimental model of epileptogenesis, is induced by repetitive administration of subconvulsive amount of excitatory drugs. Kindled mice do not typically display spontaneous recurrent seizures, but are instead characterized by enhanced seizure susceptibility to convulsive stimulations. In order to provide insights into the aberrant synaptic plasticity during kindling, this study investigated the effect of pentylenetetrazol (PTZ) kindling on filamentous actin (F-actin) in mossy fiber synapses in C57BL/6 mice. Phalloidin labeling of F-actin showed that F-actin puncta were increased in number in the stratum lucidum of CA3 region in the hippocampus after kindling. The rearrangement of F-actin seemed to occur presynaptically, since synapsin I, a specific marker for mossy fiber terminals, was also up-regulated. Such subtle structural modifications occurring in the synapses are thought to contribute to the long-lasting increased sensitivity in the PTZ-kindled C57BL/6 mice.
机译:化学点燃作为癫痫发生的实验模型,是通过反复服用亚惊厥量的兴奋性药物来诱导的。 Kindle小鼠通常不表现出自发性反复发作,而是以惊厥刺激引起的癫痫发作敏感性增强为特征。为了提供有关点燃过程中异常突触可塑性的见解,本研究调查了戊烯四唑(PTZ)点燃对C57BL / 6小鼠苔藓纤维突触中丝状肌动蛋白(F-actin)的影响。鬼笔环肽标记的F-肌动蛋白表明,点燃后海马CA3区的透明层中F-肌动蛋白的点数增加。 F-肌动蛋白的重排似乎在突触前发生,因为苔藓纤维末端的特异性标记突触素I也被上调。这种在突触中发生的细微结构修饰被认为有助于PTZ型C57BL / 6小鼠持久提高敏感性。

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