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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The neurotrophin receptor p75~(NTR) modulates long-term depression and regulates the expression of AMPA receptor subunits in the hippocampus
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The neurotrophin receptor p75~(NTR) modulates long-term depression and regulates the expression of AMPA receptor subunits in the hippocampus

机译：神经营养因子受体p75〜（NTR）调节长期抑郁症并调节海马AMPA受体亚基的表达

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摘要

Neurotrophins are involved in the modulation of synaptic transmission, including the induction of long-term potentiation (LTP) through the receptor TrkB. Because previous studies have revealed a bidirectional mode of neurotrophin action by virtue of signaling through either the neurotrophin receptor p75~(NTR) or the Trk receptors, we tested the hypothesis that p75~(NTR) is important for long-term depression (LTD) to occur. Although LTP was found to be unaffected in hippocampal slices of two different strains of mice carrying mutations of the p75~(NTR) gene, hippocampal LTD was impaired in both p75~(NTR)-deficient mouse strains. Furthermore, the expression levels of two (RS)-α-amino-3-hydroxy-5-methyl-4-iso-xazolepropionic acid (AMPA) receptor subunits, GluR2 and GluR3, but not GluR1 or GluR4, were found to be significantly altered in the hippocampus of p75~(NTR)-deficient mice. These results implicate p75~(NTR) in activity-dependent synaptic plasticity and extend the concept of functional antagonism of the neurotrophin signaling system.
机译：神经营养蛋白参与突触传递的调节，包括通过受体TrkB诱导长期增强（LTP）。因为先前的研究已经揭示了通过通过神经营养蛋白受体p75〜（NTR）或Trk受体发出的信号来表达神经营养蛋白的双向模式，所以我们检验了p75〜（NTR）对于长期抑郁症（LTD）重要的假设。发生。尽管发现LTP在携带p75〜（NTR）基因突变的两种不同品系小鼠的海马切片中不受影响，但在这两种p75〜（NTR）缺陷小鼠品系中海马LTD均受损。此外，发现两个（RS）-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体亚基GluR2和GluR3的表达水平显着，但不是GluR1或GluR4。 p75〜（NTR）缺陷小鼠海马的改变。这些结果暗示p75〜（NTR）依赖于活动的突触可塑性，并扩展了神经营养蛋白信号系统的功能拮抗作用的概念。

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