Identifying New Antimigraine Targets: Lessons from Molecular Biology

Neuroimaging experiments propose that the migraine attack originates in hypothalamus. A further mismatch communication or tuning of trigeminovascular system, might lead to calcitonin gene-related peptide (CGRP) release, sensitization, and pain.Potential targets for CGRP include middle meningeal artery, satellite glial cells, importantly Aδ neurons. The receptor is also expressed node Ranvier, current hypothesis recognizes this novel site as a regulator excitability.At molecular level, new can be found among modulators excitability, both on C fibers (to prevent neuropeptide release) reduce action potential generation sensitization), with being GPCRs ion channels localized at Ranvier. Primary headaches are one most common conditions; prevalent. Recent work pathophysiology suggests leading sensitization release (CGRP). In Opinion, we use up-to-date understanding mechanisms behind pain, provide aspects how modify system development future treatments; acute well prophylactic. We explore distribution expression neuropeptides themselves, certain channels, they may act concert excitability trigeminal neurons represent up 300 separate diagnoses, prevalent these, prevalence 15% global population. It predominant women (two three times more than men) frequent active ages (18–50 years) [1.Headache Classification Committee International Headache Society Disorders, 3rd edn.Cephalalgia. 2018; 38: 1-211Crossref PubMed Scopus (1535) Google Scholar,2.Feigin V.L. et al.The burden neurological disorders: translating evidence into policy.Lancet Neurol. 2020; 19: 255-265Abstract Full Text PDF (69) Scholar]. Studies diseases, injuries, risk factors have demonstrated cause years life lived disabilities under 50s sexes [3.Steiner T.J. al.Migraine first disability 50s: will health politicians now take notice?.J. 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