Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex
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Sidorov-2015-Metabotropic glutama.pdf
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Author(s) • • • •
Kaplan, Eitan S.
Lindemann, Lothar
Sidorov, Michael
Osterweil, Emily
Bear, Mark
Date Issued
October 2015
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Sidorov, Michael S., Eitan S. Kaplan, Emily K. Osterweil, Lothar Lindemann, and Mark F. Bear. “Metabotropic Glutamate Receptor Signaling Is Required for NMDA Receptor-Dependent Ocular Dominance Plasticity and LTD in Visual Cortex.” Proc Natl Acad Sci USA 112, no. 41 (September 28, 2015): 12852–12857.
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Final published version
Abstract
A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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DOI of Published Version
https://doi.org/10.1073/pnas.1512878112