Tapas K Makar, Volodymyr Gerzanich, Vamshi K C Nimmagadda, Rupal Jain, Kristal Lam, Fahad Mubariz, David Trisler, Svetlana Ivanova, Seung Kyoon Woo, Min Seong Kwon, Joseph Bryan, Christopher T Bever, J Marc Simard
BACKGROUND: In experimental autoimmune encephalomyelitis (EAE), deletion of transient receptor potential melastatin 4 (Trpm4) and administration of glibenclamide were found to ameliorate disease progression, prompting speculation that glibenclamide acts by directly inhibiting Trpm4. We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression...
November 18, 2015: Journal of Neuroinflammation