Immunoelectron microscopic study of tubulin and microtubule-associated proteins after transient cerebral ischemia in gerbils
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Updated: Oct 13, 2026
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
1Department of Neurology, Mayo Clinic, Rochester, MN 55905.
Abstract:
Differential vulnerability of microtubule components to cerebral ischemia has been reported previously. We investigated the disintegration of microtubules using immunoelectron microscopy for alpha-tubulin and microtubule-associated protein 1A and 2 (MAP1A and 2). Mongolian gerbils were subjected to bilateral carotid occlusion for 10 to 30 min and reperfusion for up to 72 h following ischemia for 10 min. After ischemia for 10 min, some dendrites in the stratum moleculare of the subiculum-CA1 region lost immunoreaction products for alpha-tubulin and MAPs. Loss of the reaction products spread to the medial CA1 region during progressive ischemia for 30 min. In some dendrites, electron-dense precipitates for MAPs were dispersed in the dendritic cytoplasm with little reaction product on microtubules and without alteration of the reaction for alpha-tubulin. After recirculation, loss of electron-dense precipitates for alpha-tubulin and MAPs, as well as disintegration of microtubules, propagated further to the medial CA1 region and to the proximal dendrites. The present study demonstrated prompt disintegration of microtubules with rapid disappearance of the reaction for MAPs which seemed to be caused by detachment of MAPs from the microtubule cores.
Insights
Cerebral ischemia rapidly disintegrates microtubules, particularly affecting microtubule-associated proteins (MAPs). This detachment of MAPs from microtubule cores precedes structural damage, highlighting a key mechanism in ischemic neuronal injury.
Area of Science:
- Neuroscience
- Cell Biology
- Ischemic Stroke Research
Background:
- Microtubule integrity is crucial for neuronal structure and function.
- Cerebral ischemia differentially affects microtubule components.
- Previous studies indicate vulnerability of microtubules to ischemic conditions.
Purpose of the Study:
- To investigate the disintegration process of microtubules following cerebral ischemia.
- To examine the roles of alpha-tubulin and microtubule-associated proteins (MAP1A and MAP2) in this process.
- To elucidate the temporal and spatial progression of microtubule damage and MAP detachment.
Main Methods:
- Immunoelectron microscopy was used to visualize alpha-tubulin and MAP1A/MAP2.
- Mongolian gerbils underwent transient bilateral carotid occlusion (10-30 min) followed by reperfusion (up to 72 h).
- Analysis focused on the subiculum-CA1 region, specifically dendrites in the stratum moleculare.
Main Results:
- Early ischemia (10 min) caused loss of alpha-tubulin and MAP immunoreactivity in some dendrites.
- MAP detachment from microtubule cores occurred, leading to cytoplasmic dispersion of MAPs, preceding alpha-tubulin changes.
- Reperfusion exacerbated microtubule disintegration and MAP loss, propagating damage to proximal dendrites and medial CA1 regions.
Conclusions:
- Microtubule disintegration is a rapid consequence of cerebral ischemia.
- The detachment of MAPs from microtubule cores is an early event, preceding significant alpha-tubulin alterations.
- This MAP detachment mechanism is a primary contributor to microtubule instability and subsequent neuronal damage during ischemia-reperfusion.
