Super-delayed changes of muscarinic acetylcholine receptor in the gerbil hippocampus following transient ischemia.

Super-delayed changes of muscarinic acetylcholine receptor in the gerbil hippocampus following transient ischemia.
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短暂性缺血后沙鼠海马毒蕈碱乙酰胆碱受体的超延迟变化。

DOI:
10.1007/978-1-4684-5907-4_28
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发表时间:
1991
影响因子:
--
通讯作者:
A. Mori
A. Mori
中科院分区:
医学4区
文献类型:
--
作者:
N. Ogawa;K. Haba;M. Asanuma;K. Mizukawa;A. Mori

文献摘要

被引文献

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由于许多神经元死亡而导致的血管性痴呆等脑血管病后遗症病例逐渐增多。脑缺血后的这种神经元死亡被认为是由于呼吸链受损导致的能量缺乏。然而,对迟发性神经元死亡的分析表明,神经元死亡不仅仅是由能量缺乏引起的。关于迟发性神经元死亡的研究主要集中在急性至亚急性期的形态学变化和能量代谢方面。关于慢性期的生化变化,特别是神经递质受体的变化,报道很少。
Cases of sequelae of cerebrovascular disease such as vascular dementia due to death of many neurons have been gradually increasing. Such neuronal death following brain ischemia has been considered to be due to energy deficiency resulting from an impaired respiratory chain. However, analysis of the delayed neuronal death showed that neuronal death is not caused by mere energy deficiency. Most studies on delayed neuronal death focused on the morphological changes and energy metabolism in the acute to subacute stage. There are few reports concerning biochemical changes in the chronic stage, especially in neurotransmitter receptors.