Morphological changes in CA3 pyramidal neurons after transient global ischemia.

IF 1.7 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2025-10-01 Epub Date: 2025-08-08 DOI:10.1097/WNR.0000000000002206

Xia Hu, Zhi Guo, Zhongshan Shi, Peilin Zhen, Meijuan Zhou

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引用次数: 0

Abstract

Background: Transient global cerebral ischemia induces selective neuronal death, with pyramidal neurons in the hippocampal CA1 region degenerating while CA3 neurons remain intact. Although dendritic and spine alterations in CA1 neurons postischemia have been extensively studied, the morphological changes in surviving CA3 neurons remain poorly understood.

Methods: Using Golgi staining and three-dimensional reconstruction in a rat four-vessel occlusion ischemia model, we examined dendritic and spine dynamics in CA3 neurons. In addition, P0 cultured hippocampal neurons transfected with green fluorescent protein (GFP) were exposed to oxygen-glucose deprivation (OGD) in vitro , and dendritic morphological changes were monitored longitudinally.

Results: Transient ischemia triggered apical dendritic retraction in CA3 neurons 48 h post-injury, while basal dendrites remained unaffected. Apical dendritic branching also decreased at this time point. Spine density transiently increased at 12 and 24 h before normalizing by 48 h, with no significant shift in spine type proportions. In-vitro, surviving primary hippocampal neurons showed delayed dendritic shortening post-OGD, whereas degenerating neurons exhibited early dendritic elongation.

Conclusion: Surviving CA3 pyramidal neurons exhibit greater adaptability to ischemic stress compared with vulnerable CA1 neurons, possibly explaining their differential survival. Pharmacological stabilization of neuronal morphology may offer a promising therapeutic strategy for ischemic stroke.

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短暂性全脑缺血后CA3锥体神经元的形态学改变。

背景：短暂性脑缺血引起选择性神经元死亡，海马CA1区锥体神经元变性，而CA3神经元保持完整。尽管已经对CA1神经元缺血后的树突和脊柱改变进行了广泛的研究，但对存活的CA3神经元的形态学变化仍然知之甚少。方法：采用高尔基染色法和三维重建法，观察大鼠四血管闭塞缺血模型CA3神经元的树突和脊柱动态变化。此外，将转染绿色荧光蛋白（GFP）的P0培养海马神经元体外氧糖剥夺（OGD）处理，纵向监测树突形态变化。结果：CA3神经元损伤48 h后，短暂性缺血可引起顶端树突收缩，而基底树突未受影响。顶端树突分支也在这个时间点减少。脊柱密度在12和24小时短暂增加，48小时后恢复正常，脊柱类型比例无明显变化。在体外实验中，存活的海马原代神经元在ogd后表现出延迟的树突缩短，而退化的神经元则表现出早期的树突延长。结论：存活的CA3锥体神经元比易感的CA1神经元对缺血应激表现出更强的适应性，这可能解释了CA3锥体神经元的差异存活。神经形态的药理稳定可能为缺血性脑卒中的治疗提供了一种有前途的治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.