Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons

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	Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons
	He, LM ; Chen, LY ; Lou, XL ; Qu, AL ; Zhou, Z ; Xu, T
刊名	BRAIN RESEARCH
	2002
卷号	939 期号:40910 页码:65-75
关键词	beta-amyloid peptide calcium channel calcium store ALZHEIMERS-DISEASE INTRACELLULAR CA2+ PRECURSOR PROTEIN CHANNEL FORMATION OXIDATIVE STRESS CORTICAL-NEURONS CELLS NEURODEGENERATION MECHANISM FORMS
ISSN号	0006-8993
通讯作者	Xu, T (reprint author), Huazhong Univ Sci & Technol, Inst Biophys & Biochem, Wuhan 430074, Peoples R China,
英文摘要	Accumulation of beta-amyloid (Abeta) protein in brain is an important characteristic for the etiology of Alzheimer's disease. Of all the possible processes generating the neurotoxic effects by Abeta, disruption of intracellular Ca2+ homeostasis is the primary event. In this process, various intracellular Ca2+ regulatory mechanisms are reported to be involved. Using patch-clamp techniques, both low and high voltage activated Ca2+ channel currents were recorded in the cultured dorsal root ganglion (DRG) neurons. Application of Abeta protein fragment, Abeta(25-35) (2 muM), for 30 s increased the amplitude in both currents. The Abeta-triggered facilitation effect of Ca2+ channel was found in all the depolarized potentials tested, as shown in the current-voltage relationship. Furthermore, after applying single cell Ca2+ microfluorometric method, it was found that Abeta(25-35) alone Could trigger elevations of intracellular Ca2+ concentration ([Ca2+](i)) level in 90% of the cells tested. The elevation diminished completely by cumulatively adding CdCl2, NiCl2, thapsigargin (TG), FCCP and ZN(2+) in the normal bath solution. Combining pharmacological approaches, we found that voltage-dependent Ca2+ channels, Ca2+ stores and a putative Zn2+-sensitive extracellular Ca2+ entry, respectively, makes 61.0, 25.1, and 13.9% contribution to the [Ca2+](i) increase caused by Abeta. When tested in a Ca2+-free buffer, mitochondria was found to contribute 41.3% of Abeta produced [Ca2+](i) elevation and the remaining 58.7% was attributed to endoplasmic reticulum (ER) release. (C) 2002 Elsevier Science B.V. All rights reserved.
学科主题	Neurosciences & Neurology
收录类别	SCI
语种	英语
公开日期	2012-07-23
内容类型	期刊论文
源URL	[http://ir.sibs.ac.cn/handle/331001/2056]
专题	上海神经科学研究所_神经所(总)
推荐引用方式 GB/T 7714	He, LM,Chen, LY,Lou, XL,et al. Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons[J]. BRAIN RESEARCH,2002,939(40910):65-75.
APA	He, LM,Chen, LY,Lou, XL,Qu, AL,Zhou, Z,&Xu, T.(2002).Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons.BRAIN RESEARCH,939(40910),65-75.
MLA	He, LM,et al."Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons".BRAIN RESEARCH 939.40910(2002):65-75.