
Targeting Voltage-Dependent Calcium Channels with Pregabalin Exerts a Direct Neuroprotective Effect in an Animal Model of Multiple Sclerosis
Author(s) -
Petra Hundehege,
Juncal FernándezOrth,
Pia Römer,
Tobias Ruck,
Thomas Müntefering,
Susann Eichler,
Manuela Cerina,
Lisa Epping,
Sarah Albrecht,
Amélie F Menke,
Katharina Birkner,
Kerstin Göbel,
Thomas Budde,
Frauke Zipp,
Heinz Wiendl,
Ali Gorji,
Stefan Bittner,
Sven G. Meuth
Publication year - 2018
Publication title -
neurosignals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.755
H-Index - 67
eISSN - 1424-8638
pISSN - 1424-862X
DOI - 10.1159/000495425
Subject(s) - pregabalin , neuroprotection , medicine , experimental autoimmune encephalomyelitis , multiple sclerosis , neuroscience , neuroinflammation , microglia , pharmacology , neuropathic pain , inflammation , anesthesia , immunology , biology
Multiple sclerosis (MS) is a prototypical autoimmune central nervous system (CNS) disease. Particularly progressive forms of MS (PMS) show significant neuroaxonal damage as consequence of demyelination and neuronal hyperexcitation. Immuno-modulatory treatment strategies are beneficial in relapsing MS (RMS), but mostly fail in PMS. Pregabalin (Lyrica®) is prescribed to MS patients to treat neuropathic pain. Mechanistically, it targets voltage-dependent Ca2+ channels and reduces harmful neuronal hyperexcitation in mouse epilepsy models. Studies suggest that GABA analogues like pregabalin exert neuroprotective effects in animal models of ischemia and trauma.