Host: The Japanese Society of Toxicology
Name : The 51st Annual Meeting of the Japanese Society of Toxicology
Date : July 03, 2024 - July 05, 2024
For pain to function as a biological defense mechanism, it is necessary to generate pain commensurate with the intensity and quality of noxious stimuli by accurately detecting these stimuli at nociceptors and by appropriately activating the pain signaling neural pathway from the nociceptors to the brain. However, pain varies greatly depending on physical and psychological factors and is often not commensurate with the stimulus. One typical example is allodynia (pain produced by touch stimuli), which develops after damage to the somatosensory nervous system. Such pain is thought to be caused by structural and functional changes in the somatosensory system. These changes occur not only in neurons but also in glial cells. Previous studies have shown that microglia activated soon after nerve injury produce and release proinflammatory cytokines, chemokines, and neurotrophic factors, which induce abnormal neuronal function and the onset of chronic pain. It is known that after the onset of pain, the number of microglia gradually decreases, but we have recently found that a subset of microglia with a characteristic gene expression pattern (CD11c+) appears after the pain onset. Interestingly, mice with depletion of these cells showed prolonged persistence of pain behavior. These results suggest that the roles of microglia in the onset and chronicity of nerve injury-induced pain is not uniform and that the pain chronicity may depend on the number and function of the microglial subset that emerges after nerve injury. Thus, the microglial subset will provide an important clue to elucidate the mechanisms of chronic pain and to develop new analgesics.
