Interferon-β1a protects neurons against mitochondrial toxicity via modulation of STAT1 signaling: Electrophysiological evidence

摘要: Multiple sclerosis, one of the main causes non-traumatic neurological disability in young adults, is an inflammatory and neurodegenerative disorder central nervous system. Although pathogenesis neuroaxonal damage occurring during course disease still largely unknown, there accumulating evidence highlighting potential role mitochondria multiple sclerosis-associated neuronal degeneration. The aim present study was to investigate, by utilizing electrophysiological techniques brain striatal slices, protective effects interferon-β1a, most widely used medication for against acute dysfunction induced mitochondrial toxins. Interferon-β1a found exert a dose-dependent effect progressive loss field amplitude complex I inhibitor rotenone. also reduced generation rotenone-induced inward current spiny neurons. Conversely, interferon-β1a did not influence II 3-nitropropionic acid. inhibition be dependent on activation STAT1 signaling. endogenous dopamine depletion modulation p38 MAPK mTOR pathways interferon-β1a. During experimental autoimmune encephalomyelitis (EAE) rotenone toxicity enhanced but evident. These results support future studies investigating played specific intracellular signaling mediating link among inflammation, impairment degeneration sclerosis.