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

This Article Full Text Full Text (PDF) All Versions of this Article: 276/49/45564    most recent M108757200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kelly, A. Articles by Lynch, M. A. Search for Related Content PubMed PubMed Citation Articles by Kelly, A. Articles by Lynch, M. A. Social Bookmarking                      What's this?

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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