PRESERVED NEUROTRANSMITTER RECEPTOR-BINDING FOLLOWING ISCHEMIA IN PRECONDITIONED GERBIL BRAIN
PRESERVED NEUROTRANSMITTER RECEPTOR-BINDING FOLLOWING ISCHEMIA IN PRECONDITIONED GERBIL BRAIN
复制标题
DOI：
10.1016/0361-9230(92)90074-8
复制
发表时间：
1992-09-01
影响因子：
3.8
通讯作者：
KOGURE, K
中科院分区：
文献类型：
--
作者：
KATO, H;ARAKI, T;KOGURE, K
用亚致死性缺血预处理大脑可诱导对随后的缺血性损伤的耐受性。使用[H-3]苯苯甲酸奎宁环酯 (QNB)、[H-3]MK 801、[H-3]环己基腺苷、[H-3]蝇蕈醇和[H-3]PN200-110，我们研究了沙鼠海马在有或没有预处理的缺血后神经递质受体和钙通道结合的变化。两分钟的前脑缺血不会产生神经元损伤，除了 CA1 亚区中的 [H-3]QNB 结合略有减少外，结合没有改变。三分钟的缺血破坏了大部分 CA1 锥体细胞，并导致 CA1 中所有使用的配体的结合减少。尽管 [H-3]QNB 和 [H-3]PN200-110 结合在再灌注早期短暂减少，表明下调，但先进行 2 分钟缺血预处理，然后再灌注 4 天，可防止 CA1 神经元损伤并防止结合减少。因此，预处理可以防止神经传递系统受损以及组织病理学神经元死亡。
Preconditioning the brain with sublethal ischemia induces tolerance to subsequent ischemic insult. Using [H-3]quinuclidinyl benzilate (QNB), [H-3]MK 801, [H-3]cyclohexyladenosine, [H-3]muscimol, and [H-3]PN200-110, we investigated the alterations in neurotransmitter receptor and calcium channel binding in the gerbil hippocampus following ischemia with or without preconditioning. Two-minute forebrain ischemia, which produced no neuronal damage, resulted in no alterations in binding except for a slight reduction in [H-3]QNB binding in the CA1 subfield. Three-minute ischemia destroyed the majority of CA1 pyramidal cells and caused, in CA1, reductions in binding of all ligands used. Preconditioning with 2-min ischemia followed by 4 days of reperfusion protected against CA1 neuronal damage and prevented the reductions in binding although [H-3]QNB and [H-3]PN200-110 binding transiently decreased in the early reperfusion period, suggesting down-regulation. Thus, preconditioning protects against damage to the neurotransmission system as well as histopathological neuronal death.