期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 2, 页码 751-756出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0708092105
关键词
cytokine; depression; neurogenesis
资金
- NIMH NIH HHS [R01 MH045481, 2 P01 MH25642, R37 MH045481, P01 MH025642, MH45481] Funding Source: Medline
Stress decreases neurogenesis in the adult hippocampus, and blockade of this effect is required for the actions of antidepressants in behavioral models of depression. However, the mechanisms underlying these effects of stress have not been identified. Here, we demonstrate an essential role for the proinflammatory cytokine IL-1 beta. Administration of IL-1 beta or acute stress suppressed hippocampal cell proliferation. Blockade of the IL-1 beta receptor, IL-1RI, by using either an inhibitor or IL-1RI null mice blocks the antineurogenic effect of stress and blocks the anhedonic behavior caused by chronic stress exposure. In vivo and in vitro studies demonstrate that hippocampal neural progenitor cells express IL-1RI and that activation of this receptor decreases cell proliferation via the nuclear factor-kappa B signaling pathway. These findings demonstrate that IL-1 beta is a critical mediator of the antineurogenic and depressive-like behavior caused by acute and chronic stress.
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