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Research Article
Yan-Chao Li
College of Basic Medical Sciences, Norman Bethune Health Science Center of Jilin University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2884-9829
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This work is licensed under a CC BY 4.0 License. Read Full License
Transient global cerebral ischemia induces acute loss of dendritic spines of CA1 pyramidal neurons in the hippocampus. On the other hand, it is unclear how the presynaptic terminals, which had lost their postsynaptic contacts, are persistently preserved after ischemia. We modeled global cerebral ischemia with two-stage 4-vessel-occlusion in rats, and found that three postsynaptic markers, MAP2, PSD95, and F-actin, were all severely decreased in area CA1 after ischemia/reperfusion (I/R). No significant change was detected for synapsin I, a presynaptic marker, at the protein level in the CA1 region after I/R. However, the puncta size of synapsin I became slightly, but significantly reduced in the early stage of I/R. As time went on, the puncta number of synapsin I became moderately decreased, while the puncta size of synaspin I was significantly increased. Interestingly, some enlarged puncta of synapsin I were observed to terminate directly onto the dendritic shafts of CA1 pyramidal cells. Due to a severe decrease of F-actin in the dendritic spines, the ratio of synapsin I/F-actin puncta number became significantly increased after I/R. The decrease in puncta size of synapsin I in the early stage of I/R may be the result of excessive release of synaptic vesicles due to I/R-induced hyperexcitability in CA3 pyramidal cells, while the increase in puncta size of synapsin I in the later stage of I/R may reflect the disability of synaptic vesicle release due to the loss of postsynaptic contacts.
Keywords
Dendritic spine, F-actin, synapsin I, transient cerebral ischemia, hippocampus
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This is a preprint. It has not completed peer review.
Research Article
Yan-Chao Li
College of Basic Medical Sciences, Norman Bethune Health Science Center of Jilin University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2884-9829
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 30 Mar, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Neurology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Transient global cerebral ischemia induces acute loss of dendritic spines of CA1 pyramidal neurons in the hippocampus. On the other hand, it is unclear how the presynaptic terminals, which had lost their postsynaptic contacts, are persistently preserved after ischemia. We modeled global cerebral ischemia with two-stage 4-vessel-occlusion in rats, and found that three postsynaptic markers, MAP2, PSD95, and F-actin, were all severely decreased in area CA1 after ischemia/reperfusion (I/R). No significant change was detected for synapsin I, a presynaptic marker, at the protein level in the CA1 region after I/R. However, the puncta size of synapsin I became slightly, but significantly reduced in the early stage of I/R. As time went on, the puncta number of synapsin I became moderately decreased, while the puncta size of synaspin I was significantly increased. Interestingly, some enlarged puncta of synapsin I were observed to terminate directly onto the dendritic shafts of CA1 pyramidal cells. Due to a severe decrease of F-actin in the dendritic spines, the ratio of synapsin I/F-actin puncta number became significantly increased after I/R. The decrease in puncta size of synapsin I in the early stage of I/R may be the result of excessive release of synaptic vesicles due to I/R-induced hyperexcitability in CA3 pyramidal cells, while the increase in puncta size of synapsin I in the later stage of I/R may reflect the disability of synaptic vesicle release due to the loss of postsynaptic contacts.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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