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锂-匹罗卡品诱导的癫痫持续状态(PISE)后海马CA1区钠钾氯共转运体1(NKCC1)和钾氯共转运体2(KCC2)的长期表达变化

Long-term expressional changes of Na+ -K+ -Cl- co-transporter 1 (NKCC1) and K+ -Cl- co-transporter 2 (KCC2) in CA1 region of hippocampus following lithium-pilocarpine induced status epilepticus (PISE).

作者信息

Li Xiubin, Zhou Jueqian, Chen Ziyi, Chen Shuda, Zhu Feiqi, Zhou Liemin

机构信息

Neurological Department of the 1st Affiliated Hospital of Sun Yat-sen University, GuangZhou, 510080, PR China.

出版信息

Brain Res. 2008 Jul 24;1221:141-6. doi: 10.1016/j.brainres.2008.04.047. Epub 2008 Apr 27.

Abstract

NKCC1 and KCC2 are encoded by slc12 gene family and involved in the maintenance of intracellular chloride concentration which may be associated with epileptogenesis. In this study, we aimed to investigate the long-term expression profiles of NKCC1 and KCC2 in CA1 region in the mice model of lithium-pilocarpine induced status epilepticus (PISE) and their relationship with epileptogenesis. We found NKCC1 mRNA and proteins were up-regulated at 1 d, 14 d and 45 d after pilocarpine injection, while KCC2 was down-regulated. According to obtained results, there were some expressional changes of NKCC1 and KCC2. Deregulation of their expression may break the balance of intracellular and extracellular chloride concentration which contributes to the mechanism of hyperexcitability leading to seizures. Also it may provide new drug targets for development of new antiepileptic medicine.

摘要

NKCC1和KCC2由slc12基因家族编码,参与细胞内氯离子浓度的维持,这可能与癫痫发生有关。在本研究中,我们旨在研究在匹罗卡品诱导的癫痫持续状态(PISE)小鼠模型中,CA1区NKCC1和KCC2的长期表达谱及其与癫痫发生的关系。我们发现,匹罗卡品注射后1天、14天和45天,NKCC1的mRNA和蛋白表达上调,而KCC2表达下调。根据所得结果,NKCC1和KCC2存在一些表达变化。它们表达的失调可能会打破细胞内外氯离子浓度的平衡,这有助于导致癫痫发作的过度兴奋机制。这也可能为开发新型抗癫痫药物提供新的药物靶点。

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