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点燃发展的分子基础分析。

Analyses of the molecular basis of kindling development.

作者信息

McNamara J O

机构信息

Department of Medicine (Neurology) and Neurobiology, Duke University Medical Center, North Carolina 27710, USA.

出版信息

Psychiatry Clin Neurosci. 1995 Jun;49(3):S175-8. doi: 10.1111/j.1440-1819.1995.tb02167.x.

DOI:10.1111/j.1440-1819.1995.tb02167.x
PMID:8612137
Abstract

Kindling has become the most widely studied animal model of limbic epilepsy. Understanding the molecular basis of kindling development may provide novel therapeutic approaches to prevention of limbic epileptogenesis. I briefly describe the kindling model and outline the basis for my thinking that kindling represents a synaptic reorganization triggered by pathologic activity in the mature nervous system. The pathologic activity is postulated to evoke a cascade of gene expression driven, at least in part, by glutamate receptor activation. Evidence in support of this hypothesis is presented, as are future challenges that permit critical tests of these ideas.

摘要

点燃效应已成为研究最为广泛的边缘性癫痫动物模型。了解点燃效应发展的分子基础可能会为预防边缘性癫痫发生提供新的治疗方法。我简要描述一下点燃效应模型,并概述我认为点燃效应代表成熟神经系统中由病理活动触发的突触重组这一观点的依据。据推测,这种病理活动会引发一系列至少部分由谷氨酸受体激活驱动的基因表达。文中给出了支持这一假说的证据,以及能够对这些观点进行关键验证的未来挑战。

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1
Analyses of the molecular basis of kindling development.点燃发展的分子基础分析。
Psychiatry Clin Neurosci. 1995 Jun;49(3):S175-8. doi: 10.1111/j.1440-1819.1995.tb02167.x.
2
The relevance of kindling for human epilepsy.点燃效应与人类癫痫的相关性。
Epilepsia. 2007;48 Suppl 2:65-74. doi: 10.1111/j.1528-1167.2007.01068.x.
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Neuroplasticity in specific limbic system circuits may mediate specific kindling induced changes in animal affect-implications for understanding anxiety associated with epilepsy.特定边缘系统回路中的神经可塑性可能介导动物中特定点燃诱导的情绪变化——对理解与癫痫相关的焦虑的启示。
Neurosci Biobehav Rev. 2000 Sep;24(7):705-23. doi: 10.1016/s0149-7634(00)00032-4.
4
[Cellular-molecular mechanisms of kindling].[点燃的细胞分子机制]
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Synaptic plasticity in kindling.点燃效应中的突触可塑性
Adv Neurol. 1999;79:631-43.
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The molecular basis of kindling.点燃的分子基础。
Brain Pathol. 1993 Oct;3(4):395-403. doi: 10.1111/j.1750-3639.1993.tb00767.x.
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Null mutation of c-fos impairs structural and functional plasticities in the kindling model of epilepsy.c-fos基因的无效突变会损害癫痫点燃模型中的结构和功能可塑性。
J Neurosci. 1996 Jun 15;16(12):3827-36. doi: 10.1523/JNEUROSCI.16-12-03827.1996.
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Does kindling model anything clinically relevant?点燃模型是否能模拟任何具有临床相关性的情况?
Biol Psychiatry. 1990 Feb 1;27(3):249-79. doi: 10.1016/0006-3223(90)90001-i.
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[Neuronal plasticity associated with learning and epileptic seizures: LTP and KIP].[与学习和癫痫发作相关的神经元可塑性:长时程增强和Kindling]
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Pharmacology of glutamate receptor antagonists in the kindling model of epilepsy.癫痫点燃模型中谷氨酸受体拮抗剂的药理学
Prog Neurobiol. 1998 Apr;54(6):721-41. doi: 10.1016/s0301-0082(97)00092-0.

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