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. 2022 Sep 28;13:944791. doi: 10.3389/fneur.2022.944791

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Copyright © 2022 Salahi, Parsa, Nourmohammadi, Razmkhah, Salimi, Rahmani, Zivary, Askarzadeh, Tapak, Vaezi, Sadeghsalehi, Yaghoobpoor, Mottahedi, Garousi and Deravi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Neuroinflammation and migraine. Stimulation of the trigeminal neurons causes the release of neuropeptides, including CGRP, substance P (SP), leading to mast cell degranulation, leukocyte infiltration, glial cell activation, and increased production of inflammatory TNF-α, IL-1, and IL-6 cytokines. Besides, satellite glial cells (SGCs) and trigeminal ganglions (TG) express receptors for CGRP, and CGRP can stimulate intracellular signaling molecules that are relevant to pain, such as cAMP, CREB, MAPK, and ERK. Under the influence of inflammation, activated microglia, T cells, and mast cells can boost the inflammation loop and production of cytotoxic mediators in the CNS.