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J. Biol. Chem., Vol. 276, Issue 49, 45564-45572, December 7, 2001

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The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1 on Long Term Potentiation
A ROLE FOR JNK^*

Áine Kelly, Aileen Lynch, Emily Vereker, Yvonne Nolan, Patrice Queenan, Elizabeth Whittaker, Luke A. J. O'Neill, and Marina A. Lynch^§

From the Trinity College Institute of Neuroscience, Department of Physiology and  Department of Biochemistry, Trinity College, Dublin 2, Ireland

Several effects of the proinflammatory cytokine, interleukin-1 (IL-1), have been described in the central nervous system, and one area of the brain where marked changes have been reported is the hippocampus. Among these changes are an IL-1-induced inhibition of long term potentiation (LTP) in perforant path-granule cell synapses and an attenuation of glutamate release in synaptosomes prepared from the hippocampus. Evidence suggests that, at least in circulating cells, the anti-inflammatory cytokine, IL-10, antagonizes certain effects of IL-1. We investigated the effect of IL-10 on IL-1-induced inhibition of LTP and glutamate release. The evidence presented indicates that IL-1 stimulates the stress-activated protein kinase, c-Jun-activated protein kinase (JNK), and IL-1 receptor-associated kinase, which may explain its inhibitory effect on release and LTP, and that IL-10 reversed the IL-1-induced stimulation of JNK activity and inhibition of release and LTP. We observed that IL-10 abrogated the stimulatory effect of IL-1 on superoxide dismutase activity and reactive oxygen species production, whereas the H₂O₂-induced inhibition of LTP was also blocked by IL-10. We present evidence that suggests that the action of IL-10 may be mediated by its ability to induce shedding of the IL-1 type I receptor.

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