Abstract：
Epileptic seizures are seen as a result of changing excitability balance depending on the deterioration in synaptic plasticity in the brain. Neuroplastin, and its related molecules which are known to play a role in synaptic plasticity, neurotransmitter activities that provide balance of excitability and, different neurological diseases, have not been studied before in epilepsy. In this study, a total of 34 Sprague-Dawley male and female rats, 2 months old, weighing 250-300 g were used. The epilepsy model in rats was made via pentylenetetrazole (PTZ). After the completion of the experimental procedure, the brain tissue of the rats were taken and the histopathological changes in the hippocampus and cortex parts and the brain stem were investigated, as well as the immunoreactivity of the proteins related to the immunohistochemical methods. As a result of the histopathological evaluation, it was determined that neuron degeneration and the number of dilated blood vessels in the hippocampus, frontal cortex, and brain stem were higher in the PTZ status epilepticus (SE) groups than in the control groups. It was observed that neuroplastin and related proteins TNF receptor-associated factor 6 (TRAF6), Gamma amino butyric acid type A receptors [(GABA(A)], and plasma membrane Ca2+ ATPase (PMCA) protein immunoreactivity levels increased especially in the male hippocampus, and only AMPA receptor subunit type 1 (GluA1) immunoreactivity decreased, unlike other proteins. We believe this may be caused by a problem in the mechanisms regulating the interaction of neuroplastin and GluA1 and may cause problems in synaptic plasticity in the experimental epilepsy model. It may be useful to elucidate this mechanism and target GluA1 when determining treatment strategies.
摘要：
癫痫发作被视为兴奋性平衡变化的结果，这取决于大脑中突触可塑性的恶化。神经激酶,以及已知在突触可塑性中起作用的相关分子，提供兴奋性平衡的神经递质活动，不同的神经系统疾病，以前没有在癫痫中研究过。在这项研究中,共有34只Sprague-Dawley雄性和雌性大鼠，2个月大,使用重250-300g。用戊四氮(PTZ)制作大鼠癫痫模型。实验程序完成后，取大鼠脑组织,观察海马、皮质部位和脑干的组织病理学改变,以及与免疫组织化学方法相关的蛋白质的免疫反应性。作为组织病理学评估的结果，确定神经元变性和海马中扩张的血管数量，额叶皮质,PTZ癫痫持续状态（SE）组的脑干高于对照组。观察到神经激酶和相关蛋白TNF受体相关因子6（TRAF6），γ-氨基丁酸A型受体[（GABA（A）]，和质膜Ca2ATPase（PMCA）蛋白免疫反应性水平增加，尤其是在雄性海马中，只有AMPA受体亚基1型（GluA1）免疫反应性降低，与其他蛋白质不同。我们认为这可能是由调节神经激酶和GluA1相互作用的机制中的问题引起的，并且可能导致实验性癫痫模型中突触可塑性的问题。在确定治疗策略时，阐明这种机制和靶向GluA1可能是有用的。
