Journal
MULTIPLE SCLEROSIS JOURNAL
Volume 18, Issue 11, Pages 1633-1635Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1352458512440207
Keywords
Glutamate; excitotoxicity; IL-1 beta; IPSC; neurodegeneration
Categories
Funding
- Italian National Ministero della Salute
- Fondazione TERCAS
- Fondazione Italiana Sclerosi Multipla (FISM)
- Novartis
- Teva
- Merck Serono
- Bayer Schering
- Sanofi-aventis
- Biogen Idec
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Abnormal glutamate-dependent synaptic excitation contributes to neuronal damage in multiple sclerosis (MS). Little is known about the involvement of the GABA system in this disorder. Here we found that cerebrospinal fluid (CSF) from MS patients with enhanced brain lesions on magnetic resonance imaging inhibited GABA transmission in mouse brain slices. Enhanced IL-1 beta neuronal action was responsible for this effect, because IL-1 beta receptor antagonist blocked, and exogenous IL-1 beta mimicked the synaptic effect of inflamed CSF. Our results provide evidence that focal inflammation in MS perturbs the cytokine milieu within the circulating CSF, resulting in diffuse GABAergic alteration in neurons.
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