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Updated: Aug 11, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Microglial expression of chemokine receptor CCR5 during rat forebrain development and after perinatal
Rita M Cowell1, Haiyan Xu, Jack M Parent
1Department of Neurology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Abstract:
The chemokine macrophage inflammatory protein 1alpha (CCL3) is expressed by immune cells in the normal and injured perinatal brain. To determine whether the chemokine receptor CCR5 is a relevant target for CCL3 in the brain, we used RT-PCR and immunocytochemistry to assess changes in CCR5 expression and localization in developing normal and injured rat forebrain. CCR5 protein was expressed predominately by resting and activated microglia until 2 weeks of age. Neonatal hypoxia-ischemia increased CCR5 mRNA expression while causing CCR5 internalization, indicating receptor activation. These data implicate CCR5 in microglial recruitment and activation during brain development and after neonatal brain injury.
Insights
Macrophage inflammatory protein 1alpha (CCL3) targets the CCR5 receptor on microglia in the developing brain. Neonatal injury activates CCR5, suggesting its role in microglial response during brain development and injury.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Macrophage inflammatory protein 1alpha (CCL3) is present in the perinatal brain.
- The role of its receptor, CCR5, in brain development and injury is not fully understood.
Purpose of the Study:
- To investigate CCR5 expression and localization in the developing rat forebrain.
- To determine if CCR5 is a target for CCL3 in the normal and injured perinatal brain.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) to assess mRNA expression.
- Immunocytochemistry to evaluate CCR5 protein localization.
- Analysis in normal and hypoxia-ischemia injured rat pups.
Main Results:
- CCR5 protein was primarily found on microglia in the developing rat brain up to 2 weeks of age.
- Neonatal hypoxia-ischemia increased CCR5 mRNA levels.
- Hypoxia-ischemia also induced CCR5 internalization, indicating receptor activation.
Conclusions:
- CCR5 is expressed by microglia in the developing brain.
- CCR5 activation is implicated in microglial recruitment and activation following neonatal brain injury.
- CCR5 represents a potential therapeutic target for neonatal brain injury.
