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

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