Kainic acid-induced focal cortical seizure is associated with an increase of synaptophysin immunoreactivity in the cortex.
Kainic acid-induced focal cortical seizure is associated with an increase of synaptophysin immunoreactivity in the cortex.
复制标题
红藻氨酸诱导的局灶性皮质癫痫与皮质中突触素免疫反应性的增加有关。
DOI：
10.1006/exnr.1996.0135
复制
发表时间：
1996
影响因子：
5.3
通讯作者：
Snead3rd,OC
中科院分区：
文献类型：
--
作者：
Chen,LS;Wong,JG;Banerjee,PK;Snead3rd,OC
在癫痫动物模型中，癫痫发作后齿状回颗粒上层苔藓纤维终末的异常神经发芽一直被观察到。在取自患有海马硬化症的癫痫患者的海马中也观察到。异常的神经芽生和突触重组是癫痫发生的细胞机制之一。目前尚不清楚癫痫发作活动是否能在皮层（如海马）中诱导异常突触发生。在这项研究中，突触末梢在皮质局灶性皮质癫痫发作后，通过半定量图像分析突触素免疫反应。短暂的皮质内灌注红藻氨酸诱发局灶性癫痫持续状态和破坏性皮质病变。在红藻氨酸灌注的区域，突触素免疫反应性显著增加。在局灶性皮质癫痫发作后2周和4周，观察到突触素免疫反应性增加，表明突触发生增加。这一结果表明，红藻氨酸诱导的癫痫发作活动与皮层中持久的突触发生有关。对异常突触发生的生理后果的研究可能会导致对皮层癫痫发生机制的进一步理解。
Aberrant neural sprouting of mossy fiber terminals in the supragranular layer of dentate gyrus is consistently observed following seizures in an animal model of epilepsy. It is also observed in hippocampi taken from epileptic patients with hippocampal sclerosis. The aberrant neural sprouting with synaptic reorganization is one of the proposed cellular mechanisms underlying epileptogenesis. It is not known whether aberrant synaptogenesis can be induced in the cortex, as in hippocampus, by seizure activity. In this study, synaptic terminals in the cortex were measured after focal cortical seizures by a semiquantitative image analysis of synaptophysin immunoreactivity. Brief intracortical perfusion of kainic acid induced focal status epilepticus and destructive cortical lesions. Synaptophysin immunoreactivity was significantly increased in the area where kainic acid was perfused. The increase of synaptophysin immunoreactivity, indicating an increase of synaptogenesis, was observed at 2 and 4 weeks after focal cortical seizures. This result suggests that kainic acid-induced seizure activity is associated with long-lasting synaptogenesis in the cortex. Studies centering on the physiological consequences of aberrant synaptogenesis may lead to additional understanding of the mechanisms underlying cortical epileptogenesis.