Araki T, Kato H, Kanai Y, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Neuroscience. 1993 Apr;53(3):829-36. doi: 10.1016/0306-4522(93)90627-r.
Receptor autoradiographic and histological techniques were used to investigate the long-term changes that occur in the gerbil brain following the induction of transient cerebral ischemia. Transient ischemia was induced for 3 and 10 min, and animals were allowed to survive for eight months. Autoradiographic analysis of second messenger systems showed that 3-min ischemia caused a significant reduction in [3H]inositol-1,4,5-trisphosphate binding in the hippocampal CA1 sector, whereas the alteration in [3H]phorbol 12,13-dibutyrate, [3H]forskolin and [3H] cyclic-AMP bindings was not found in this region. In the striatum, 3-min ischemia caused no significant alteration in [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]forskolin binding sites, whereas the [3H]cyclic-AMP binding showed a significant elevation. The thalamus exhibited a significant elevation only in the [3H]inositol-1,4,5-trisphosphate binding sites. Following 10-min ischemia, [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]cyclic-AMP binding sites revealed a significant reduction in the hippocampus, whereas the [3H]forskolin binding showed a significant elevation in this area. In the striatum, 10-min ischemia caused no significant alteration in [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]cyclic-AMP binding sites. However, marked reduction in the [3H]forskolin binding was seen in the striatum. Furthermore, the substantia nigra also exhibited a significant reduction in [3H]forskolin binding. Histological studies suggested that 3-min ischemia can produce severe neuronal damage and mild shrinkage to the hippocampal CA1 sector. They also showed that 10-min ischemia can cause severe tissue shrinkage and severe neuronal damage in the hippocampal CA1 sector and hippocampal CA3 sector. Thus, the hippocampal damage following ischemia was not static but progressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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诱导后发生的长期变化。诱导短暂性缺血3分钟和10分钟，让动物存活8个月。对第二信使系统的放射自显影分析表明，3分钟缺血导致海马CA1区[3H]肌醇-1,4,5-三磷酸结合显著减少，而该区域未发现[3H]佛波醇12,13-二丁酸、[3H]福司可林和[3H]环磷酸腺苷结合的改变。在纹状体中，3分钟缺血导致[3H]佛波醇12,13-二丁酸、[3H]肌醇-1,4,5-三磷酸和[3H]福司可林结合位点无显著改变，而[3H]环磷酸腺苷结合显著升高。丘脑仅在[3H]肌醇-1,4,5-三磷酸结合位点有显著升高。10分钟缺血后，海马中[3H]佛波醇12,13-二丁酸、[3H]肌醇-1,4,5-三磷酸和[3H]环磷酸腺苷结合位点显著减少，而该区域[3H]福司可林结合显著升高。在纹状体中，10分钟缺血导致[3H]佛波醇12,13-二丁酸、[3H]肌醇-1,4,5-三磷酸和[3H]环磷酸腺苷结合位点无显著改变。然而，纹状体中[3H]福司可林结合显著减少。此外，黑质中[3H]福司可林结合也显著减少。组织学研究表明，3分钟缺血可导致海马CA1区严重的神经元损伤和轻度萎缩。研究还表明，10分钟缺血可导致海马CA1区和海马CA3区严重的组织萎缩和严重的神经元损伤。因此，缺血后海马损伤并非静止不变，而是进行性的。（摘要截断于250字）
