Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology.

Abstract

Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive, abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential (TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion, TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular, activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective anti-migraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.

• Authors: Mamoru Shibata, Chunhua Tang
• Journal: Neuroscience bulletin (Neurosci Bull) Vol. 37 Issue 1 Pg. 103-116 (Jan 2021) ISSN: 1995-8218 [Electronic] Singapore
• PMID: 32870468 (Publication Type: Journal Article, Review)

Chemical References

• Transient Receptor Potential Channels
• Calcitonin Gene-Related Peptide

Topics

• Calcitonin Gene-Related Peptide (metabolism)
• Humans
• Migraine Disorders
• Neurons (metabolism)
• Transient Receptor Potential Channels
• Trigeminal Ganglion (metabolism)