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Updated: Feb 11, 2026

Simultaneous Imaging of Microglial Dynamics and Neuronal Activity in Awake Mice
Published on: August 23, 2022
Loss of neuronal CD200 contributed to microglial activation after acute cerebral ischemia in mice
Yang Yang1, Xiang-Jian Zhang1, Cong Zhang1
1Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; Hebei Key Laboratory of Vascular Homeostasis and Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, 215 Hepingxi Road, Shijiazhuang, 050000, Hebei, PR China.
Abstract:
CD200 has been proved to play a role in immuno-inflammatory reaction. However, little information is available on CD200 in the acute stage of cerebral ischemia. We investigated the association between neuronal death and expression of CD200, and explored the relationship between CD200 and microglia in cerebral ischemic mice. Firstly, localization of CD200 expression in the normal brain tissue was detected by immunofluorescent assay. Then, focal cerebral ischemia was induced in mice by permanent middle cerebral artery occlusion (pMCAO) and then cortical tissues were collected at 6, 12, 24 and 48 h after surgery. Changes of CD200 and neuron-specific enolase (NSE) after pMCAO were assessed by western blotting. Meanwhile flow cytometry analysis was implemented to analyze the death of cortical cells. Results of these two parts were analyzed by Pearson correlation analysis. To further study, intracerebroventricular (ICV) injection of recombinant CD200 (rCD200) protein was carried out immediately after pMCAO. Iba-1 was measured by western blotting to evaluate activation of microglia, and inflammatory cytokines including IL-1β, TNF-α and IL-10 were tested by enzyme-linked immuno sorbent assay (ELISA). The results showed that CD200 was expressed in neurons and was not observed on mircroglia in cortex of normal mice. Expression of CD200 was decreased within 48 h after pMCAO, with a concomitant decrease of NSE expression. The rate of neuronal cell death was approximately around 30% and statistical analysis revealed a negative correlation between level of CD200 and the rate of neuronal death. Compared with control, exogenous rCD200 reduced expressions of Iba-1, IL-1β, TNF-α and IL-10. Taking together, our results demonstrated that loss of CD200 was caused by neuronal death and was one of contributing factors in microglial activation after cerebral ischemia. ICV injection of rCD200 protein could suppress activation of microglia in vivo.
Insights
Loss of CD200 in neurons correlates with neuronal death after cerebral ischemia. Administering recombinant CD200 (rCD200) protein reduced microglial activation and inflammation in ischemic mice.
Area of Science:
- Neuroscience
- Immunology
Background:
- CD200 plays a role in immuno-inflammatory responses.
- Limited data exists on CD200's role in acute cerebral ischemia.
Purpose of the Study:
- Investigate the association between CD200 expression and neuronal death in cerebral ischemia.
- Explore the relationship between CD200 and microglia activation post-ischemia.
Main Methods:
- Induced focal cerebral ischemia in mice (pMCAO).
- Assessed CD200, neuron-specific enolase (NSE), and microglial activation (Iba-1) via Western blotting.
- Analyzed neuronal cell death using flow cytometry and inflammatory cytokines (IL-1β, TNF-α, IL-10) via ELISA.
- Administered intracerebroventricular recombinant CD200 (rCD200) protein post-ischemia.
Main Results:
- CD200 is expressed in neurons, not microglia, in normal brain tissue.
- CD200 and NSE expression decreased post-pMCAO, correlating negatively with neuronal death rate.
- Exogenous rCD200 administration reduced microglial activation markers and inflammatory cytokines.
Conclusions:
- CD200 loss is linked to neuronal death and contributes to microglial activation in cerebral ischemia.
- Recombinant CD200 (rCD200) shows potential in suppressing microglial activation and inflammation in ischemic conditions.
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