Early and Late Neuronal Damage Following Cerebral Ischemia
Early and Late Neuronal Damage Following Cerebral Ischemia
复制标题
脑缺血后的早期和晚期神经元损伤
DOI:
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发表时间:
1988
期刊:
影响因子:
--
通讯作者:
K. Sano
中科院分区:
文献类型:
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作者:
T. Kirino;A. Tamura;K. Sano
The hippocampus is one of the most vulnerable structures in the brain to ischemia. It is been widely believed that the hippocampus is most easily subject to neuronal death and “sclerosis” following only a brief period of ischemia of merely a few minutes. However, neurophysiologists have long been using the hippocampal slice method for their experiments. They know that their in vitro slice preparation of the hippocampus obtained mainly from rodent species is surprisingly normal and remains normal for many hours (Lynch, 1980). In this procedure, hippocampal tissue is unavoidably exposed to brief ischemia during preparation until it is cut into slices. The experience of neurophysiologists may, therefore, confirm that hippocampal neurons, if any, are only on rare occasions destroyed rapidly following brief ischemia. These seemingly contradictory observations may be resolved by the recognition of delayed neuronal death in the hippocampus. Most of the hippocampal CA1 neurons die following brief ischemia, but cell disintegration takes place very slowly (Kirino, 1982; Pulsinelli et al., 1982). It takes almost days until overt morphological signs of neuronal death appear. As the brain is subjected to longer ischemia, this neuronal cell alteration develops faster following recirculation (Kirino and Sano, 1984a). This general tendency of neuronal pathology is describled by Ito et al. and called “maturation phenomenon” (Ito et al., 1975). In the rodent hippocampus, delayed neuronal death is most commonly encountered in animals which survive longer than a few days following ischemia. On the other hand, ischemia which is long enough to cause widespread acute cell change in the hippocampus is usually incompatible with animal survival.
影响因子:
1.9
作者:
Wieloch,T;Lindvall,O;Blomqvist,P;Gage,FH
通讯作者:
Gage,FH