Behavioral stress modifies hippocampal synaptic plasticity through corticosterone-induced sustained extracellular signal-regulated kinase/mitogen-activated protein kinase activation

Chih Hao Yang, Chiung Chun Huang, Kuei Sen Hsu

研究成果: 雜誌貢獻文章同行評審

139 引文 斯高帕斯(Scopus)

摘要

The induction of hippocampal long-term synaptic plasticity is exquisitely sensitive to behavioral stress, but the underlying mechanisms are still unclear. We report here that hippocampal slices prepared from adult rats that had experienced unpredictable and inescapable restraint tail-shock stress showed marked impairments of long-term potentiation (LTP) in the CA1 region. The same stress promoted the induction of long-term depression (LTD). These effects were prevented when the animals were given the glucocorticoid receptor antagonist 11β,17β-11[4-(dimethylamino)phenyl]-17-hydroxy-17-(1-propynyl) -estra-4-9-dien-3-one before the stress. Immunoblotting analyses revealed that stress induced a profound and prolonged extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK1/2 MAPK) hyperphosphorylation through small GTPase Ras, Raf-1, and MAPK kinase 1/2 (MEK1/2). Furthermore, the stress effects were obviated by the intrahippocampal injection of specific inhibitors of MEK1/2 (U0126), protein kinase C (bisindolylmaleimide I), tyrosine kinase (K252a), and BDNF antisense oligonucleotides. These results suggest that the effects of stress on LTP and LTD originate from the corticosterone-induced sustained activation of ERK1/2-coupled signaling cascades.
原文英語
頁(從 - 到)11029-11034
頁數6
期刊Journal of Neuroscience
24
發行號49
DOIs
出版狀態已發佈 - 十二月 8 2004
對外發佈Yes

ASJC Scopus subject areas

  • Neuroscience(all)

指紋 深入研究「Behavioral stress modifies hippocampal synaptic plasticity through corticosterone-induced sustained extracellular signal-regulated kinase/mitogen-activated protein kinase activation」主題。共同形成了獨特的指紋。

引用此