Mitochondrial calcium function and dysfunction in the central nervous system.
Mitochondrial calcium function and dysfunction in the central nervous system.
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DOI：
10.1016/j.bbabio.2009.03.010
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发表时间：
2009-11
影响因子：
4.3
通讯作者：
Nicholls, David G.
中科院分区：
文献类型：
--
作者：
Nicholls, David G.
分离的脑线粒体积累、储存和释放钙的能力已被广泛表征。外推到完整的神经元导致预测，在原位线粒体将可逆地积累Ca2+的浓度时，在线粒体附近的阳离子的浓度上升超过“设定点”，在该“设定点”的摄取和流出是在平衡，存储Ca2+与磷酸盐的复合物，并缓慢释放阳离子时，质膜离子泵降低细胞质游离Ca2+。预计阳离子的过度积累会导致渗透性转变的激活，对神经元造成灾难性后果。这些预测中的每一个都已经用完整的神经元证实，并且有令人信服的证据表明细胞Ca 2+过载中的渗透性转变与谷氨酸兴奋性毒性和中风相关，而其中线粒体Ca 2+处理中可能的缺陷已经被最深入地研究的神经退行性疾病是亨廷顿病。在这个简短的审查证据，线粒体Ca2+转运相关的神经元的生存在这些条件下将进行讨论。
The ability of isolated brain mitochondria to accumulate, store and release calcium has been extensively characterized. Extrapolation to the intact neuron led to predictions that the in situ mitochondria would reversibly accumulate Ca2+ when the concentration of the cation in the vicinity of the mitochondria rose above the ‘set-point’ at which uptake and efflux were in balance, storing Ca2+ as a complex with phosphate, and slowly releasing the cation when plasma membrane ion pumps lowered the cytoplasmic free Ca2+. Excessive accumulation of the cation was predicted to lead to activation of the permeability transition, with catastrophic consequences for the neuron. Each of these predictions has been confirmed with intact neurons, and there is convincing evidence for the permeability transition in cellular Ca2+ overload associated with glutamate excitotoxicity and stroke, while the neurodegenerative disease in which possible defects in mitochondrial Ca2+ handling have been most intensively investigated is Huntington's Disease. In this brief review evidence that mitochondrial Ca2+ transport is relevant to neuronal survival in these conditions will be discussed.
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影响因子：
4.7
作者：
Brustovetsky, N;LaFrance, R;Dubinsky, JM
通讯作者：
Dubinsky, JM
影响因子：
3
作者：
Bambrick, Linda L.;Chandrasekaran, Krish;Fiskum, Gary
通讯作者：
Fiskum, Gary
影响因子：
4.8
作者：
Chalmers, S;Nicholls, DG
通讯作者：
Nicholls, DG
DOI：
10.1073/pnas.83.16.6179
发表时间：
1986-08-01
影响因子：
11.1
作者：
CONNOR, JA
通讯作者：
CONNOR, JA
影响因子：
4
作者：
Bolshakov, Alexey P.;Mikhailova, Maria M.;Khodorov, Boris I.
通讯作者：
Khodorov, Boris I.