Hippocampal neuronal damage and its possible mechanism in status epilepticus
10.3760/cma.j.issn.2095-428X.2015.24.005
- VernacularTitle:癫(痫)持续状态模型中海马神经元损伤及其可能机制
- Author:
Xiufang DING
;
Jiwen WANG
;
Guo YAO
;
Fangfang DAI
;
Bing ZHANG
- Publication Type:Journal Article
- Keywords:
Status epilepticus;
Hippocampus;
α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor;
Glyceral dehyde-3-phosphate dehydrogenase
- From:
Chinese Journal of Applied Clinical Pediatrics
2015;30(24):1855-1858
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate hippocampal neuronal damage and dynamic change of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunit GluR2 in status epilepticus, to find out whether GluR2/glyceral dehyde-3-phosphate dehydrogenase (GAPDH) interaction has any change.Methods Male Wistar rats (62 cases) were induced to status epilepticus by using LiC1-pilocarpine.The 62 rats were divided into 1 h (6 cases),6 h (12 cases), 24 h (12 cases),72 h (12 cases)and 7 d (20 cases)after status epilepticus.At the same time, the healthy control group (12 cases) was established.Morphologic changes of hippocampus and the amount of apoptotic cells in healthy control and SE model groups at different time points (6 h, 24 h, 72 h, 7 d) (6 cases each group) after status epilepticus were quantified by adopting Nissl staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining respectively.Expressions of GluR2 in healthy control and SE model groups at 1 h,6 h,24 h,72 h and 7 d (6 cases each group) after status epilepticus were detected by using Western blot.Co-precipitation and Western blot techniques were used to investigate whether the GluR2/GAPDH interaction in the hippocampus was increased.Results Compared with the healthy control group, the number of nerve cells in the hippocampal CA1 and CA3 regions was significantly reduced at all studied time points(F =30.866,24.043, all P ＜0.05).Apoptotic cells in hippocampal CA1 and CA3 regions were significantly increased at 24 h,72 h and 7 d after status epilepticus (F =84.762,52.574, all P ＜ 0.01).GluR2 at 1 h,6 h after status epilepticus was equal to that of the control group (P ＞ 0.05), but it was shown to be significantly down-regulated at other studied time points (F =76.506,P ＜ 0.01);when compared with the healthy control group,the GluR2/GAPDH interaction was significantly up-regulated in the hippocampus at 72 h after status epilepticus (t =7.029, P ＜ 0.05).Conclusions Status epilepticus can lead to neuronal damage in the hippocampus.Down-regulation of GluR2 and increase of the GluR2/GAPDH complex formation might be one of the mechanisms involved in hippocampal neuronal damage.
