Related Experiment Video
Updated: Aug 9, 2026
Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord
Published on: February 22, 2015
Imaging the peripheral benzodiazepine receptor response in central nervous system demyelination and remyelination
Ming-Kai Chen1, Tomás R Guilarte
1Molecular Neurotoxicology Laboratory, Department of Environmental Health Sciences, The Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland 21205, USA.
Abstract:
We used a rodent model of cuprizone-induced demyelination to examine the peripheral benzodiazepine receptor (PBR) response during remyelination. C57BL/6J mice were fed a 0.2% cuprizone-containing or control diet for 3 weeks and then removed to allow for remyelination. Quantitative autoradiography of 3H-(R)-PK11195 binding to PBR in the corpus callosum showed increased levels at 3 weeks of demyelination and gradually decreased as a function of remyelination. PBR levels were associated with the degree of remyelination and activation of microglia and astrocytes. However, the temporal pattern suggests that the PBR signal during the late stages of remyelination was primarily associated with astrocytes. We also used small-animal positron-emission tomography (PET) imaging to determine if this technique could be used to monitor PBR levels in the brain of living mice. The results indicate that 11C-(R)-PK11195 levels are significantly elevated in the mouse brain during cuprizone-induced demyelination and normalize at a time in which remyelination is complete. These findings support the notion that PBR is a sensitive marker for the visualization and quantification of brain injury and recovery. Further, the in vivo imaging of the PBR response is now possible in the living rodent brain.
Insights
Peripheral benzodiazepine receptor (PBR) levels increase during demyelination and decrease during remyelination. Positron-emission tomography (PET) imaging can monitor PBR in living rodent brains, aiding in visualizing brain injury and recovery.
Area of Science:
- Neuroscience
- Neuroinflammation
- Demyelinating Diseases
Background:
- Cuprizone-induced demyelination is a common rodent model for studying myelin repair.
- Peripheral benzodiazepine receptors (PBR) are implicated in neuroinflammation and glial cell activation.
Purpose of the Study:
- To investigate the role of PBR in demyelination and remyelination using a rodent model.
- To assess the utility of positron-emission tomography (PET) imaging for monitoring PBR in vivo.
Main Methods:
- Rodents were subjected to cuprizone-induced demyelination followed by a remyelination period.
- Quantitative autoradiography with 3H-(R)-PK11195 was used to measure PBR binding in brain tissue.
- Small-animal PET imaging with 11C-(R)-PK11195 was employed to visualize PBR in living mice.
Main Results:
- PBR levels in the corpus callosum were elevated during demyelination and decreased during remyelination.
- PBR levels correlated with the extent of remyelination and glial cell activation (microglia and astrocytes).
- PET imaging revealed elevated 11C-(R)-PK11195 levels during demyelination, which normalized upon remyelination completion.
Conclusions:
- PBR serves as a sensitive marker for brain injury and recovery in demyelinating conditions.
- In vivo PET imaging is a viable method for monitoring PBR dynamics in the living rodent brain.
- PBR imaging holds potential for tracking disease progression and therapeutic efficacy in neurological disorders.
