Onodera H, Aoki H, Yae T, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Neuroscience. 1990;38(1):125-36. doi: 10.1016/0306-4522(90)90379-i.
The hippocampus provides a suitable area in the brain for the analysis of neuronal plasticity after application of a selective lesioning technique. Using histochemistry and autoradiography, we studied synaptic reorganization in the rat hippocampus with selective CA1 pyramidal cell lesioning caused by transient forebrain ischemia after long-term survival. An autoradiographic study was performed on second messenger systems ([3H]inositol 1,4,5-trisphosphate, [3H]forskolin and [3H]phorbol 12,13-dibutyrate binding). One-hundred days after ischemia, depletion of CA1 pyramidal cells and marked shrinkage of the CA1 subfield was noted in spite of unaltered thickness of the CA3 band and of the dentate molecular layers. Although neuronal density in the CA3 region of animals killed seven days after ischemia was not different from the normal group, 78% of animals showed neuronal loss of 30-50% in the stratum pyramidale of the CA3b 100 days after recirculation. Sixty-seven per cent of animals exhibited supragranular mossy fiber sprouting in the dentate gyrus. However, CA3 neuronal loss did not correlate with mossy fiber sprouting. Succinic dehydrogenase was depleted in the CA1 100 days after ischemia, and animals with CA3 damage showed a reduction of succinic dehydrogenase activity in the CA3. In contrast to the unaltered acetylcholinesterase in the animals killed seven days after ischemia, high density bands of acetylcholinesterase activity in the stratum pyramidale of the CA1 were found to be broadened 100 days after ischemia. In the CA1 subfield, subnormal activity of [3H]phorbol 12,13-dibutyrate and [3H]forskolin binding were observed in spite of the depleted [3H]inositol 1,4,5-triphosphate binding. [3H]Forskolin binding in the hilus had increased by 62% 100 days after ischemia, although binding in the stratum lucidum of the CA3 and in the stratum moleculare of the dentate gyrus was unaltered. However, no visible supragranular increase in [3H]forskolin binding was observed. These results indicate that long-term survival after CA1 pyramidal cell depletion caused by transient forebrain ischemia induced the modulation of neuronal activity and synaptic rearrangements in the whole hippocampal formation.
海马体为大脑提供了一个合适的区域，可用于在应用选择性损伤技术后分析神经元可塑性。我们使用组织化学和放射自显影技术，研究了长期存活后由短暂性前脑缺血导致的选择性CA1锥体细胞损伤的大鼠海马体中的突触重组。对第二信使系统（[3H]肌醇1,4,5 - 三磷酸、[3H]福斯高林和[3H]佛波酯12,13 - 二丁酸结合）进行了放射自显影研究。缺血后100天，尽管CA3带和齿状分子层厚度未改变，但仍观察到CA1锥体细胞减少以及CA1亚区明显萎缩。尽管缺血后7天处死的动物CA3区域的神经元密度与正常组无差异，但再灌注100天后，78%的动物在CA3b的锥体层出现30 - 50%的神经元丢失。67%的动物在齿状回出现颗粒上苔藓纤维发芽。然而，CA3神经元丢失与苔藓纤维发芽并无关联。缺血后100天，CA1中的琥珀酸脱氢酶减少，而CA3受损的动物在CA3中琥珀酸脱氢酶活性降低。与缺血后7天处死的动物中乙酰胆碱酯酶未改变形成对比的是，缺血后100天发现CA1锥体层中乙酰胆碱酯酶活性的高密度带变宽。在CA1亚区，尽管[3H]肌醇1,4,5 - 三磷酸结合减少，但仍观察到[3H]佛波酯12,13 - 二丁酸和[3H]福斯高林结合的活性低于正常水平。缺血后100天，海马门区的[3H]福斯高林结合增加了62%，尽管CA3的透明层和齿状回的分子层中的结合未改变。然而，未观察到[3H]福斯高林结合在颗粒上有明显增加。这些结果表明，短暂性前脑缺血导致CA1锥体细胞缺失后的长期存活诱导了整个海马结构中神经元活动的调节和突触重排。
