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The Journal of Neuroscience, May 28, 2008, 28(22):5752-5755; doi:10.1523/JNEUROSCI.0654-08.2008

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Brief Communications
The Glutamate Receptor-Interacting Protein Family of GluR2-Binding Proteins Is Required for Long-Term Synaptic Depression Expression in Cerebellar Purkinje Cells

Kogo Takamiya,^2,3 Lifang Mao,¹ Richard L. Huganir,^1,3 and David J. Linden³

¹Howard Hughes Medical Institute and ²Departments of Neurosurgery and ³Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Correspondence should be addressed to David J. Linden, Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

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.

Key words: glutamate; AMPA receptor; plasticity; motor learning; cerebellum; dendrite

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Received Feb. 13, 2008; revised April 14, 2008; accepted April 14, 2008.

Correspondence should be addressed to David J. Linden, Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

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