Neuroreport · 2025
Morphological changes in CA3 pyramidal neurons after transient global ischemia.
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Hu Xia, Guo Zhi, Shi Zhongshan, Zhen Peilin, Zhou Meijuan
Аннотация
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.
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.