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CX3CL1-CX3CR1 pathway mediates hyperthermia-induced microglial processes retraction
Ru Song1, Chunhua Liu1, Minqi Peng1
1Shenzhen-Hong Kong Institute of Brain Science, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China; Guangdong Provincial Key Laboratory of Brain Connectome and Behavior, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
High fever causes brain cells called microglia to retract their processes. The CX3CL1-CX3CR1 pathway, regulated by ADAM10 and NMDA receptors, is key to this fever-induced microglial change.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- High fever in infants is linked to microglial morphological changes and seizures.
- The molecular basis of microglial process retraction during hyperthermia is not well understood.
Purpose of the Study:
- To investigate the molecular mechanisms of microglial process retraction during hyperthermia.
- To identify key molecular players in fever-induced microglial activation.
Main Methods:
- Utilized a hyperthermia-induced microglial activation model in postnatal day 8 mice.
- Examined the role of the CX3CL1-CX3CR1 pathway and ADAM10.
- Investigated the involvement of glutamate and NMDA receptors.
Main Results:
- The CX3CL1-CX3CR1 interaction was identified as a critical regulator of microglial process retraction.
- ADAM10 was found to be the primary enzyme cleaving CX3CL1 under hyperthermia; its inhibition prevented process retraction.
- NMDA receptor activation mimicked hyperthermia effects, while NMDA blockers attenuated the process retraction.
Conclusions:
- The CX3CL1-CX3CR1 pathway is essential for mediating microglial process retraction in response to hyperthermia.
- ADAM10 and NMDA receptor signaling are crucial components of this fever-induced microglial response.
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