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- W4378966437 abstract "Migraines are a considerable social problem and economic burden worldwide. Current acute treatments are based on inhibiting meningeal neurogenic inflammation which has poor results in some patients, whereas the site of action of prophylactic medicines are unknown; therefore, exploring new treatment mechanisms and methods is increasingly needed. Recent evidence suggests that microglia and microglia-mediated neuroinflammation are important in migraine pathogenesis. In the cortical spreading depression (CSD) migraine model, microglia were activated after multiple CSD stimulations, suggesting that microglial activation may be associated with recurrent attacks of migraine with aura. In the nitroglycerin-induced chronic migraine model, the microglial response to extracellular stimuli leads to the activation of surface purine receptors P2X4、P2X7、P2Y12, which mediate signal transduction through intracellular signalling cascades, such as the BDNF/TrkB, NLRP3/IL-1β and RhoA/ROCK signalling pathways, and release inflammatory mediators and cytokines that enhance pain by increasing the excitability of nearby neurons. Inhibition of the expression or function of these microglial receptors and pathways inhibits the abnormal excitability of TNC (trigeminal nucleus caudalis) neurons and intracranial as well as extracranial hyperalgesia in migraine animal models. These findings suggest that microglia may be central in migraine recurrent attacks and a potential target for the treatment of chronic headaches." @default.
- W4378966437 created "2023-06-02" @default.
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- W4378966437 date "2023-08-01" @default.
- W4378966437 modified "2023-09-26" @default.
- W4378966437 title "The status of knowledge on migraines: The role of microglia" @default.
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- W4378966437 doi "https://doi.org/10.1016/j.jneuroim.2023.578118" @default.
- W4378966437 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37295033" @default.
- W4378966437 hasPublicationYear "2023" @default.
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