Status epilepticus alters hippocampal PKAβ and PKAγ expression in mice

被引:3
|
作者
Liu, Jian Xin [1 ,3 ]
Tang, Yong Cheng [1 ]
Liu, Yong [3 ]
Tang, Feng Ru [1 ,2 ]
机构
[1] Natl Univ Singapore, Temasek Labs, Singapore 117411, Singapore
[2] Natl Univ Singapore, Dept Anat, Singapore 117548, Singapore
[3] Xi An Jiao Tong Univ, Sch Med, Inst Neurobiol, Xian 710049, Peoples R China
来源
SEIZURE-EUROPEAN JOURNAL OF EPILEPSY | 2010年 / 19卷 / 07期
基金
英国医学研究理事会;
关键词
PKA; Mouse; Hippocampus; Status epilepticus; DEPENDENT PROTEIN-KINASE; MOUSE HIPPOCAMPUS; PILOCARPINE MODEL; NMDA RECEPTOR; K+ CURRENT; CA1; AREA; MODULATION; PHOSPHORYLATION; NEURONS; CHANNELS;
D O I
10.1016/j.seizure.2010.06.008
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objectives: To investigate the localization and progressive changes of cyclic-AMP dependent protein kinase (cPKA) in the mouse hippocampus at acute stages during and after pilocarpine induced status epilepticus. Methods: Pilocarpine induced status epilepticus mice were sacrificed 30 min, 2 h or 1 day after the start of a similar to 7 h lasting status as assessed by video-electroencephalography. Brains were processed for quantitative immunohistochemistry of hippocampal cPKA beta and cPKA gamma, and immunohistochemical co-localization of cPKA beta and cPKA gamma with calbindin (CB), calretinin (CR), and parvalbumin (PV). Results: Based on anatomical and morphological assessment, cPKA beta was primarily expressed by principal cells and cPKA gamma by interneurons. In CA1, cPKA beta co-localized with 76% of CB, 41% of CR. and 95% of PV-immunopositive cells, while cPKA gamma co-localized with 50% of CB, 29% of CR, and 80% of PV-immunopositive cells. Upon induction of status epilepticus, cPKA beta expression was transiently reduced in CA1, whereas cPKA gamma expression was sustainably reduced. Conclusion: cPKA may play an important role in neuronal hyperexcitability, death and epileptogenesis during and after pilocarpine induced status epilepticus. (C) 2010 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:414 / 420
页数:7
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