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J. Biol. Chem., Vol. 277, Issue 23, 20717-20723, June 7, 2002

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Opposing Roles for NF-B/Rel Factors p65 and c-Rel in the Modulation of Neuron Survival Elicited by Glutamate and Interleukin-1^*

Marina Pizzi^§, Francesca Goffi, Flora Boroni, Marina Benarese, Scott E. Perkins^¶, Hsiou-Chi Liou^**, and PierFranco Spano

From the  Division of Pharmacology and Experimental Therapeutics, Department of Biomedical Sciences and Biotechnologies, School of Medicine, University of Brescia, 25123 Brescia, Italy and the ^** Department of Microbiology and Immunology and the ^¶ Laboratory and Animal Facility, Weill Medical College of Cornell University, New York, New York 10021

The nuclear transcription factors NF-B/Rel have been shown to function as key regulators of either cell death or survival in neuronal cells. Here, we investigated whether selective activation of diverse NF-B/Rel family members might lead to distinct effects on neuron viability. In both cultured rat cerebellar granule cells and mouse hippocampal slices, we examined NF-B/Rel activation induced by two opposing modulators of cell viability: 1) interleukin-1 (IL-1), which promotes neuron survival and 2) glutamate, which can elicit toxicity. IL-1 produced a prolonged stimulation of NF-B/Rel factors by inducing both IB and IB degradation. Glutamate produced a delayed and transient activation of NF-B/Rel, which was associated with a brief loss of IB. Moreover, IL-1 activated the p50, p65, and c-Rel subunits of NF-B/Rel, whereas glutamate activated only the p50 and p65 proteins. The inhibition of NF-B/Rel protein expression by antisense oligonucleotides in cerebellar granule cells showed that p65 was involved in glutamate-mediated cell death, whereas c-Rel was essential for IL-1-preserved cell survival. Furthermore, the depletion of c-Rel in cultured neurons as well as in the hippocampus from the c-Rel^/ mouse converted the IL-1 effect into toxicity. These findings suggest that, within a single neuron, the balance between cell death and survival in response to external stimuli may rely on the activation of distinct NF-B/Rel proteins.

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