PDZ proteins interacting with C-terminal GluR2/3 are involved in a PKC-dependent regulation of AMPA receptors at hippocampal synapses

  • Neuron. 2000 Dec;28(3):873-86. doi: 10.1016/s0896-6273(00)00160-4.
M I Daw  1 ,  R Chittajallu ,  Z A Bortolotto ,  K K Dev ,  F Duprat ,  J M Henley ,  G L Collingridge ,  J T Isaac
Affiliations
  • 1. MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, University Walk, BS8 1TD, Bristol, United Kingdom.
PMID: 11163273 DOI: 10.1016/s0896-6273(00)00160-4
Abstract

We investigated the role of PDZ proteins (GRIP, ABP, and PICK1) interacting with the C-terminal GluR2 by infusing a ct-GluR2 peptide ("pep2-SVKI") into CA1 pyramidal neurons in hippocampal slices using whole-cell recordings. Pep2-SVKI, but not a control or PICK1 selective peptide, caused AMPAR-mediated EPSC amplitude to increase in approximately one-third of control neurons and in most neurons following the prior induction of LTD. Pep2-SVKI also blocked LTD; however, this occurred in all neurons. A PKC Inhibitor prevented these effects of pep2-SVKI on synaptic transmission and LTD. We propose a model in which the maintenance of LTD involves the binding of AMPARs to PDZ proteins to prevent their reinsertion. We also present evidence that PKC regulates AMPAR reinsertion during dedepression.

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