The glutamate receptor-interacting protein family of GluR2-binding proteins is required for long-term synaptic depression expression in cerebellar Purkinje cells

被引:57
作者
Takamiya, Kogo [1 ,3 ]
Mao, Lifang [2 ]
Huganir, Richard L. [1 ,2 ]
Linden, David J. [1 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Neurosurg, Baltimore, MD 21205 USA
关键词
glutamate; AMPA receptor; plasticity; motor learning; cerebellum; dendrite;
D O I
10.1523/JNEUROSCI.0654-08.2008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Glutamate receptor-interacting protein 1 (GRIP1) and GRIP2 are closely related proteins that bind GluR2-containing AMPA receptors and couple them to structural and signaling complexes in neurons. Cerebellar long-term synaptic depression (LTD) is a model system of synaptic plasticity that is expressed by persistent internalization of GluR2-containing AMPA receptors. Here, we show that genetic deletion of both GRIP1 and GRIP2 blocks LTD expression in primary cultures of mouse cerebellar neurons but that single deletion of either isoform allows LTD to occur. In GRIP1/2 double knock-out Purkinje cells, LTD can be fully rescued by a plasmid-driving expression of GRIP1 and partially rescued by a GRIP2 plasmid. These results indicate that the GRIP family comprises an essential molecular component for cerebellar LTD.
引用
收藏
页码:5752 / 5755
页数:4
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