Epilepsy is a neurological disorder characterized by the occurrence of spontaneous and recurrent seizures. In post-traumatic epilepsy (PTE), the mechanism of epileptogenesis is very complex and seems to be linked with voltage-gated ion channels. Dehydroepiandrosterone (DHEA), a neurosteroid have shown beneficial effect against various neurological disorders. We investigated antiepileptic effect of DHEA with respect to expression of voltage-gated ion channels subtypes in iron-induced epilepsy. Iron (FeCl3) solution was intracartically injected to induce epilepsy in rats and DHEA was intraperitoneally administered for 21 days. Results showed markedly increased epileptiform seizures activity along with up-regulation of Nav1.1 and Nav1.6, and down-regulation of Cav2.1α at the mRNA and protein level in the cortex and hippocampus of epileptic rats. Moreover, the study demonstrated that these channels subtypes were predominantly expressed in the neurons. DHEA treatment has countered the epileptic seizures, down-regulated Nav1.1 and Nav1.6, and up-regulated Cav2.1α without affecting their cellular localization. In conclusion, the present study demonstrates antiepileptic potential of DHEA, escorted by regulation of Nav1.1, Nav1.6, and Cav2.1α subtypes in the neurons of iron-induced epileptic rats.

中文翻译：

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电压门控钠和钙通道亚型对脱氢表雄酮治疗铁诱发癫痫的反应。

癫痫是一种神经系统疾病，其特征是发生自发性和复发性癫痫发作。在创伤后癫痫 (PTE) 中，癫痫发生的机制非常复杂，似乎与电压门控离子通道有关。脱氢表雄酮 (DHEA) 是一种神经类固醇，已显示出对各种神经系统疾病的有益作用。我们研究了 DHEA 对铁诱导癫痫中电压门控离子通道亚型表达的抗癫痫作用。铁（FeCl 3 ）溶液被注射到大鼠中以诱发癫痫，并腹腔注射DHEA 21天。结果显示癫痫样发作活动显着增加，伴随着Nav1.1和Nav1.6的上调，以及癫痫大鼠皮层和海马的mRNA和蛋白质水平的Cav2.1α的下调。此外，该研究表明这些通道亚型主要在神经元中表达。DHEA 治疗可以对抗癫痫发作，下调 Nav1.1 和 Nav1.6，上调 Cav2.1α，而不影响它们的细胞定位。总之，本研究证明了 DHEA 的抗癫痫潜力，由铁诱导的癫痫大鼠神经元中 Nav1.1、Nav1.6 和 Cav2.1α 亚型的调节护送。