Journal
NEUROPSYCHOPHARMACOLOGY
Volume 33, Issue 9, Pages 2237-2250Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.npp.1301612
Keywords
brain inflammation; cytokines; excitotoxicity; seizures; hypoxia; adenosine A(1) receptor
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The immunological response in the brain is crucial to overcome neuropathological events. Some inflammatory mediators, such as the immunoregulatory cytokine interleukin-6 (IL-6) affect neuromodulation and may also play protective roles against various noxious conditions. However, the fundamental mechanisms underlying the long-term effects of IL-6 in the brain remain unclear. We now report that IL-6 increases the expression and function of the neuronal adenosine A(1) receptor, with relevant consequences to synaptic transmission and neuroprotection. IL-6-induced amplification of A(1) receptor function enhances the responses to readily released adenosine during hypoxia, enables neuronal rescue from glutamate-induced death, and protects animals from chemically induced convulsing seizures. Taken together, these results suggest that IL-6 minimizes the consequences of excitotoxic episodes on brain function through the enhancement of endogenous adenosinergic signaling.
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