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短暂性脑缺血后沙鼠脑内神经递质受体的长期变化

Long-term changes in gerbil brain neurotransmitter receptors following transient cerebral ischaemia.

作者信息

Araki T, Kato H, Kogure K, Kanai Y

机构信息

Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Br J Pharmacol. 1992 Oct;107(2):437-42. doi: 10.1111/j.1476-5381.1992.tb12764.x.

Abstract
  1. Receptor autoradiographic and histological techniques were used to investigate long-term changes in the gerbil brain following transient cerebral ischaemia. 2. Transient ischaemia was induced for 3 min and 10 min, and the animals were allowed to survive for 8 months. 3. Histological examination revealed that 3 min ischaemia caused neuronal damage and mild shrinkage only in the hippocampal CA1 sector. Ten minutes of ischaemia produced severe neuronal damage in the striatum and the hippocampal CA1 and CA3 sectors. Considerable shrinkage was seen in the hippocampus; the dentate gyrus, however, was not damaged. 4. Three minutes of ischaemia produced changes in the binding of [3H]-quinuclidinylbenzilate ([3H]-QNB), [3H]-muscimol, and [3H]-MK-801 in various brain regions, as determined autoradiographically. In contrast, [3H]-cyclohexladenosine ([3H]-CHA) and [3H]-PN200-110 ([3H]-isradipine) binding in the brain was unaltered. 5. Ten minutes of ischaemia resulted in a major loss of neurotransmitter receptors, especially in the hippocampus. The substantia nigra showed a significant reduction in [3H]-CHA binding, whereas the striatum, which was morphologically damaged, showed no significant changes in any of the neurotransmitter receptors examined. 6. The results demonstrated that long-term survival after transient cerebral ischaemia produced alterations in neurotransmitter receptors, especially in the hippocampal formation, where considerable shrinkage was noted. These results also suggest that the hippocampal damage was not static, but progressive.
摘要
  1. 采用受体放射自显影和组织学技术研究沙土鼠脑在短暂性脑缺血后的长期变化。2. 诱导短暂性缺血3分钟和10分钟,让动物存活8个月。3. 组织学检查显示,3分钟缺血仅导致海马CA1区神经元损伤和轻度萎缩。10分钟缺血则在纹状体、海马CA1区和CA3区造成严重神经元损伤。海马出现明显萎缩;然而,齿状回未受损。4. 放射自显影测定显示,3分钟缺血导致不同脑区[3H] - 喹核醇基苯甲酸酯([3H] - QNB)、[3H] - 蝇蕈醇和[3H] - MK - 801的结合发生变化。相比之下,脑内[3H] - 环己腺苷([3H] - CHA)和[3H] - PN200 - 110([3H] - 伊拉地平)的结合未改变。5. 10分钟缺血导致神经递质受体大量丧失,尤其是在海马。黑质[3H] - CHA结合显著减少,而形态学受损的纹状体在所检测的任何神经递质受体方面均无显著变化。6. 结果表明,短暂性脑缺血后的长期存活导致神经递质受体发生改变,尤其是在海马结构,该区域出现明显萎缩。这些结果还提示,海马损伤并非静止不变,而是进行性的。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd33/1907888/7f532507dbe2/brjpharm00213-0172-a.jpg

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