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

MI Daw, R Chittajallu, ZA Bortolotto, KK Dev, F Duprat… - Neuron, 2000 - cell.com
MI Daw, R Chittajallu, ZA Bortolotto, KK Dev, F Duprat, JM Henley, GL Collingridge
Neuron, 2000cell.com
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 …
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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