TREK channel activation suppresses migraine pain phenotype
Pablo Ávalos PradoFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceArnaud Landra-WillmFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceClément VerkestFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceAurore RiberaFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceAnne‐Amandine ChassotFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceAnne BaronFédération Hospitalo-Universitaire InovPain, Cote d'Azur University, University Hospital Centre Nice, Nice, Provence-Alpes-Côte d'Azur, FranceGuillaume SandozFédération Hospitalo-Universitaire, Paris Center for Microbiome Medicine
2021en
ABI
Annotatsiya
) channels inhibits TG neuronal firing sufficiently to fully reverse the migraine-like phenotype induced by NO-donors in rodents. Finally, targeting TREK is as efficient as treatment with CGRP antagonists, which represents one of the most effective migraine therapies. Altogether, our results demonstrate that inhibiting TG excitability by pharmacological activation of TREK channels should be considered as an alternative to the current migraine treatment.
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