Related Experiment Video
Updated: Aug 2, 2026
13:28
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
TR3 death receptor expression in the normal and ischaemic brain
D C Harrison1, J Roberts, C A Campbell
1Department of Neuroscience Research, SmithKline Beecham Pharmaceuticals, Harlow, Essex, UK.
Neuroscience
|April 25, 2000
Summary
Death receptors TR3 and TR7 are expressed in the brain. TR3 levels increase globally after stroke, unlike other receptors, indicating distinct responses to ischemic injury.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Death receptors are implicated in neuronal cell death during development and disease.
- Understanding their role in the central nervous system is crucial for neurodegenerative and acute brain injury research.
Purpose of the Study:
- To investigate the expression patterns of TR3 and TR7 death receptors in the adult human and rat central nervous system.
- To analyze the modulation of death receptor expression in response to acute ischemic injury using an in vivo stroke model.
Main Methods:
- Expression analysis of TR3 and TR7 in adult human and rat brain tissue.
- In vivo rat model of permanent middle cerebral artery occlusion (MCAO) to induce stroke.
- Quantitative analysis of death receptor expression in lesioned and unlesioned brain regions post-stroke.
Main Results:
- TR3 expression is high in the human cerebellum and widespread in the rat brain.
- In the MCAO stroke model, TR3 showed a rapid, global increase in both lesioned and unlesioned brain areas.
- Tumor necrosis factor receptor 1, Fas, and p75 neurotrophin receptor (NGFR) were upregulated specifically in the lesioned cortex, while TR7 expression remained unchanged.
Conclusions:
- TR3 and TR7 exhibit distinct expression profiles in the central nervous system.
- TR3 displays a unique, global response to ischemic injury, differing from other studied death receptors.
- These findings highlight differential regulation of death receptors following ischemic brain injury.
