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Proc Natl Acad Sci U S A. 2010 Feb 9;107(6):2580-5. doi: 10.1073/pnas.0915139107. Epub 2010 Feb 1.

Inhibitory role for GABA in autoimmune inflammation.

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1
Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. roopa.bhat@stanford.edu

Abstract

GABA, the principal inhibitory neurotransmitter in the adult brain, has a parallel inhibitory role in the immune system. We demonstrate that immune cells synthesize GABA and have the machinery for GABA catabolism. Antigen-presenting cells (APCs) express functional GABA receptors and respond electrophysiologically to GABA. Thus, the immune system harbors all of the necessary constituents for GABA signaling, and GABA itself may function as a paracrine or autocrine factor. These observations led us to ask further whether manipulation of the GABA pathway influences an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). Increasing GABAergic activity ameliorates ongoing paralysis in EAE via inhibition of inflammation. GABAergic agents act directly on APCs, decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins.

PMID:
20133656
PMCID:
PMC2823917
DOI:
10.1073/pnas.0915139107
[Indexed for MEDLINE]
Free PMC Article

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