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The Journal of Neuroscience, July 21, 2004, 24(29):6482-6488; doi:10.1523/JNEUROSCI.5712-03.2004

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Development/Plasticity/Repair
Cell Type-Specific Interleukin-1 Signaling in the CNS

Deepak Srinivasan,¹ Jui-Hung Yen,¹ Donald J. Joseph,² and Wilma Friedman¹

¹Department of Biological Sciences, Rutgers University, Newark, New Jersey 07102, and ²Center for Neurobiology and Behavior, Columbia University, New York, New York 10032

Interleukin-1 (IL-1) is a potent and pleiotropic inflammatory cytokine that is highly produced in the CNS under conditions of damage, disease, or stress. This cytokine acts on CNS glia to effect inflammatory responses, mediated in part via activation of the nuclear factor-B (NF-B) transcription factor, and consequent induction of numerous cytokines. Neurons as well as astrocytes in the hippocampus also express the type 1 IL-1 receptor, indicating that this cytokine can influence neuronal function directly, yet IL-1 does not induce production of cytokines in neurons as it does in glia. In contrast, IL-1 regulates synaptic function of hippocampal neurons. Here we demonstrate that different signaling pathways mediate IL-1 actions in neurons as compared with astrocytes. IL-1 activates the p38 mitogen-activated protein kinase (MAPK) signaling pathway and induces the activation of CREB in hippocampal neurons, in contrast to the activation of NF-B in hippocampal astrocytes, demonstrating cell type-specific signaling responses to IL-1 in the brain and yielding distinct functional responses.

Key words: interleukin-1; neurons; astrocytes; NF-B; p38 MAPK; signal transduction

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Received Dec 26, 2003; revised June 7, 2004; accepted June 9, 2004.

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