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TMEM16F Regulates Spinal Microglial Function in Neuropathic Pain States
Laura Batti1, Mayya Sundukova1, Emanuele Murana2
1EMBL Mouse Biology Unit, Via Ramarini 32, Monterotondo 00015, Italy.
Cell Reports
|June 23, 2016
Summary
TMEM16F protein in spinal microglia is crucial for neuropathic pain development. Its absence prevents pain hypersensitivity by impairing microglial function and phagocytosis.
Area of Science:
- Neuroscience
- Immunology
Background:
- Neuropathic pain is a chronic pain state caused by nervous system injury.
- Spinal microglia contribute to neuropathic pain via growth factors and cytokines.
Purpose of the Study:
- Investigate the role of TMEM16F in microglial activity during neuropathic pain.
- Determine TMEM16F's function as a Ca(2+)-dependent ion channel and phospholipid scramblase in microglia.
Main Methods:
- Used conditional knockout mice lacking TMEM16F in microglia.
- Assessed mechanical hypersensitivity, microglial process motility, and phagocytosis post-nerve injury.
- Monitored GABA immunoreactivity changes.
Main Results:
- Mice lacking TMEM16F in microglia did not develop mechanical hypersensitivity.
- TMEM16F deficiency impaired microglial process motility and phagocytosis.
- Loss of GABA immunoreactivity was prevented in TMEM16F knockout mice.
Conclusions:
- TMEM16F is essential for the microglial response to nerve injury.
- Microglial phagocytosis mediated by TMEM16F is critical in neuropathic pain pathogenesis.
