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Induction of Per1 expression following an experimentally induced epilepsy in the mouse hippocampus

Authors
Eun, BokkeeKim, Hyun JungKim, Soo YoungKim, Tae WooHong, Soon TaekChoi, Kyung MiShim, Jae KwangMoon, YounghyeSon, Gi HoonKim, KyungjinKim, HyunSun, Woong
Issue Date
8-7월-2011
Publisher
ELSEVIER IRELAND LTD
Keywords
Per1; Seizure; Hippocampus; Kainic acid; Electroconvulsive shock (ECS)
Citation
NEUROSCIENCE LETTERS, v.498, no.2, pp.110 - 113
Indexed
SCIE
SCOPUS
Journal Title
NEUROSCIENCE LETTERS
Volume
498
Number
2
Start Page
110
End Page
113
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/112003
DOI
10.1016/j.neulet.2011.03.039
ISSN
0304-3940
Abstract
The Period1 (Per1) is a clock-oscillating gene product that plays an essential role in the generation and modulation of circadian rhythm in the suprachiasmatic nucleus (SCN) of hypothalamus. However, Per1 is also expressed in many other brain regions including cerebral cortex, hippocampus, and amygdala, suggesting that Pen l may be involved in the broader cellular functions in addition to the rhythm regulation. In this study, we found that chemical or electrical seizure-inducing stimulations regulate Pen 1 expression. Treatments with electric convulsive shock (ECS) or kainic acid (KA) robustly up-regulated the expressions of pen l mRNA and protein in the hippocampal formation and cerebral cortex. In consistent, we found that neuronal depolarization or KA treatment increased pen l mRNA expression in cultured primary cortical neurons. Because it has been demonstrated that Per family molecules contribute to the regulation of stress-induced cell death, we also explored the effect of Pen l overexpression on the survival of cultured neurons. However, neither basal, staurosporine- nor KA-induced neuronal death was affected by forced expression of Pert Collectively, these results suggest that the Pen l expression is neuronal activity- and epileptogen-dependent, although its functional significance is remained to be explored. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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