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Updated: May 5, 2026
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Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
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Ischemic stroke triggers brain-wide synaptic remodeling within four hours.
Huanhuan Chen1, Ye Wei1, Luminiţa Ruje2,3
1Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, Qingdao, Shandong, China.
Plos Biology
|March 2, 2026
Summary
Brain-wide synaptic rebalancing occurs within hours of stroke, with opposite changes in different brain regions. This cross-brain plasticity may be a rapid compensation mechanism in acute stroke.
Area of Science:
- Neuroscience
- Stroke Research
- Synaptic Plasticity
Background:
- The hyperacute phase of stroke (0-24 hours) involves poorly understood physiological mechanisms, hindering new therapy development.
- Synaptic plasticity's role in early stroke remains unclear, despite its known involvement in neurodegenerative and neurodevelopmental disorders.
Purpose of the Study:
- To investigate region-specific synaptic remodeling and cross-brain plasticity in the hyperacute stage of stroke.
- To elucidate the mechanisms underlying functional compensation in the early hours following ischemic stroke.
Main Methods:
- Induction of middle cerebral artery occlusion in rats to model ischemic stroke.
- Analysis of synaptic changes in ischemic core, penumbra, and contralateral cortex.
- Pharmacological blockade of NMDA-type glutamate receptors.
- Proteomic and transcriptomic analyses to assess molecular changes.
Main Results:
- Rapid synapse loss in the ischemic core and functional diminution in the penumbra within 4 hours.
- Increased synaptic staining and vesicle cycling observed in the contralateral cortex.
- NMDA receptor blockade abolished contralateral synaptic increase and worsened penumbra synaptic decline.
- Cross-brain plasticity was independent of local gene expression; penumbra showed metabolic rearrangement and synaptic downregulation.
Conclusions:
- Brain-wide synaptic rebalancing, with distinct regional changes, occurs rapidly after stroke.
- This cross-brain synaptic plasticity may represent a mechanism for functional compensation in hyperacute stroke.
- Findings highlight the brain's extensive response to acute ischemic perturbation.
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