Abstract

A REVIEW ON ROLE OF CALCITONN GENE RELATED PROTEIN ANTAGONISTS IN MIGRAINE

Pedapudi Kiran Swetha*, Hanisha Jangala, Nancy Sali, M. Tabitha Sharon, Padmalatha Kantamaneni

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Abstract

The neuropeptide calcitonin gene-related peptide (CGRP) has long been hypothesized to play an essential role in the pathophysiology of migraine. Although clinical findings are consistent with such a role, the specific pathogenic mechanism of CGRP in migraine remains speculative until recently. Advances in molecular neuroscience are beginning to elucidate the pathogenic mechanism of CGRP in migraine. This article describes the hypothetical role of CGRP in migraine and outlines current knowledge of the molecular mechanism of this neuropeptide in the pathophysiology of migraine. Studies of cultured trigeminal neurons have shown that CGRP is released from trigeminal ganglion cells, CGRP transcription is increased under conditions that mimic neuronal inflammation, migraine drug therapy reduces CGRP release, and CGRP transcription is performed. Inhibits and shows tumor necrosis factor α (TNFα). Intrinsic inflammatory mediators associated with migraine can stimulate CGRP transcription. Taken together, the results suggest that in migraine, activation of the trigeminal nerve releases CGRP and other peptides that cause the release of proinflammatory mediators. These mediators further increase CGRP synthesis and release over hours to days, corresponding to the duration of a typical migraine episode of 4 to 72 hours. Increased synthesis and release of CGRP may be mediated by activation of the mitogenactivated protein kinase pathway. It is regulated by endogenous inflammatory substances such as TNFα and can be affected by drugs such as sumatriptan.

Keywords: Headache, Migraine, Crgp, Crgp Antagonist.