NMDA receptor-dependent and metabotropic glutamate receptor-dependent forms of long-term depression coexist in CA1 hippocampal pyramidal cells
Neurobiology of Learning and Memory. 1998-07-01; 70(1-2): 62-72
DOI: 10.1006/nlme.1998.3838
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1. Neurobiol Learn Mem. 1998 Jul-Sep;70(1-2):62-72.
NMDA receptor-dependent and metabotropic glutamate receptor-dependent forms of
long-term depression coexist in CA1 hippocampal pyramidal cells.
Nicoll RA(1), Oliet SH, Malenka RC.
Author information:
(1)Department of Cellular and Molecular Pharmacology, University of California,
San Francisco, California 94143, USA.
We have found that two distinct forms of long-term depression (LTD), one
dependent on the activation of NMDA receptors (NMDARs) and the other dependent on
the activation of metabotropic glutamate receptors (mGluRs), coexist in pyramidal
cells of the CA1 region of the hippocampus of juvenile rats (11-35 days). Both
forms were pathway specific, required membrane depolarization, and were blocked
by chelating postsynaptic Ca2+ with BAPTA. The mGluR-LTD, but not the NMDAR-LTD,
was blocked by the T-type Ca2+ channel blocker Ni2+ and intracellular
administration of a protein kinase C inhibitory peptide. In contrast, the protein
phosphatase inhibitor Microcystin LR blocked NMDAR-LTD, but not mGluR-LTD.
NMDAR-LTD is associated with a decrease in the size of quantal excitatory
postsynaptic currents, whereas for mGluR-LTD there was no change in quantal size,
but a large decrease in the frequency of events. While mGluR-LTD did not interact
with NMDAR-dependent long term potentiation (LTP), NMDAR-LTD was capable of
reversing LTP. Prior saturation of mGluR-LTD had no effect on NMDAR-LTD.
NMDAR-LTD and mGluR-LTD thus appear to be mechanistically distinct forms of
synaptic plasticity in that they share neither induction nor expression
mechanisms.
Copyright 1998 Academic Press.
DOI: 10.1006/nlme.1998.3838
PMID: 9753587 [Indexed for MEDLINE]