Interleukin-1β abrogates long-term depression of hippocampal CA1 synaptic transmission

被引:35
|
作者
Ikegaya, Y
Delcroix, I
Iwakura, Y
Matsuki, N
Nishiyama, N
机构
[1] Univ Tokyo, Chem Pharmacol Lab, Grad Sch Pharmaceut Sci, Bunkyo Ku, Tokyo 1130033, Japan
[2] Univ Tokyo, Inst Med Sci, Div Cell Biol, Ctr Med Expt, Tokyo 1088639, Japan
关键词
interleukin; cytokine; lymphocyte; hippocampus synaptic plasticity; long-term potentiation; knockout mouse;
D O I
10.1002/syn.10154
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Although interleukin-1beta (IL-1beta) is well known to modulate synaptic transmission and plasticity of the hippocampus, no study has yet evaluated how this cytokine affects long-term depression (LTD), one of the major forms of hippocampal synaptic plasticity. Here we report that at Schaffer collateral-CA1 synapses, bath application of IL-1beta induces a long-lasting decrease in synaptic strength in intact slices, but not in disinhibited slices in the presence of bicuculline, a gamma-aminobutyric acid receptor antagonist. The IL-1beta-induced synaptic depression efficiently foreclosed the subsequent induction of LTD in response to a 1-Hz tetanus and, conversely, it was also prevented by preexisting LTD. These results suggest that IL-1beta-induced, persistent depression of synaptic efficacy is required for GABAergic activation and shares, at least in part, a common cellular mechanism for LTD. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:54 / 57
页数:4
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