Journal
NEURON
Volume 28, Issue 3, Pages 873-886Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(00)00160-4
Keywords
-
Categories
Funding
- Medical Research Council [G9629038] Funding Source: researchfish
- MRC [G9629038] Funding Source: UKRI
- Medical Research Council [G9629038] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available