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癫痫持续状态后钙平台期的发展:钙在癫痫发生中的作用。

Development of the calcium plateau following status epilepticus: role of calcium in epileptogenesis.

作者信息

Nagarkatti Nisha, Deshpande Laxmikant S, DeLorenzo Robert J

机构信息

Department of , Virginia Commonwealth University, Richmond, VA 23298, USA.

出版信息

Expert Rev Neurother. 2009 Jun;9(6):813-24. doi: 10.1586/ern.09.21.

Abstract

Status epilepticus is a clinical emergency defined as continuous seizure activity or rapid, recurrent seizures without regaining consciousness and can lead to the development of acquired epilepsy, characterized by spontaneous, recurrent seizures. Understanding epileptogenesis--the transformation of healthy brain tissue into hyperexcitable neuronal networks--is an important challenge and the elucidation of molecular mechanisms can lend insight into new therapeutic targets to halt this progression. It has been demonstrated that intracellular calcium increases during status epilepticus and that these elevations are maintained past the duration of the injury (Ca(2+) plateau). As an important second messenger, Ca(2+) elevations can lead to changes in gene expression, neurotransmitter release and plasticity. Thus, characterization of the post-injury Ca(2+) plateau may be important in eventually understanding the pathophysiology of epileptogenesis and preventing the progression to chronic epilepsy after brain injury.

摘要

癫痫持续状态是一种临床急症,定义为持续的癫痫发作活动或快速、反复的癫痫发作且未恢复意识,可导致获得性癫痫的发生,其特征为自发性、反复性癫痫发作。理解癫痫发生过程——即健康脑组织转变为过度兴奋的神经元网络——是一项重大挑战,阐明分子机制有助于深入了解新的治疗靶点以阻止这一进程。已经证明,在癫痫持续状态期间细胞内钙会增加,并且这些升高在损伤持续时间过后仍会维持(钙平台期)。作为一种重要的第二信使,钙升高可导致基因表达、神经递质释放和可塑性的变化。因此,损伤后钙平台期的特征描述对于最终理解癫痫发生的病理生理学以及预防脑损伤后发展为慢性癫痫可能具有重要意义。

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本文引用的文献

1
Mechanistic and pharmacologic aspects of status epilepticus and its treatment with new antiepileptic drugs.
Epilepsia. 2008 Dec;49 Suppl 9:63-73. doi: 10.1111/j.1528-1167.2008.01928.x.
2
Molecular and cellular basis of epileptogenesis in symptomatic epilepsy.
Epilepsy Behav. 2009 Jan;14 Suppl 1:16-25. doi: 10.1016/j.yebeh.2008.09.023. Epub 2008 Oct 19.
3
Convulsive status epilepticus in adults and adolescents of southwest China: mortality, etiology, and predictors of death.
Epilepsy Behav. 2009 Jan;14(1):146-9. doi: 10.1016/j.yebeh.2008.09.005. Epub 2008 Oct 31.
4
Alterations in neuronal calcium levels are associated with cognitive deficits after traumatic brain injury.
Neurosci Lett. 2008 Aug 15;441(1):115-9. doi: 10.1016/j.neulet.2008.05.113. Epub 2008 Jun 7.
6
A new potential AED, carisbamate, substantially reduces spontaneous motor seizures in rats with kainate-induced epilepsy.
Epilepsia. 2008 Oct;49(10):1787-94. doi: 10.1111/j.1528-1167.2008.01657.x. Epub 2008 May 20.
8
Levetiracetam inhibits both ryanodine and IP3 receptor activated calcium induced calcium release in hippocampal neurons in culture.
Neurosci Lett. 2008 May 16;436(3):289-93. doi: 10.1016/j.neulet.2008.02.076. Epub 2008 Mar 21.
9
Long-term decrease in calbindin-D28K expression in the hippocampus of epileptic rats following pilocarpine-induced status epilepticus.
Epilepsy Res. 2008 May;79(2-3):213-23. doi: 10.1016/j.eplepsyres.2008.02.006. Epub 2008 Apr 3.

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