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Proc Natl Acad Sci U S A. 2015 Oct 13;112(41):12852-7. doi: 10.1073/pnas.1512878112. Epub 2015 Sep 28.

Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex.

Author information

1
The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139.
2
The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139 mbear@mit.edu.

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.

KEYWORDS:

NMDA; long-term depression; mGluR5; visual cortical plasticity

PMID:
26417096
PMCID:
PMC4611661
DOI:
10.1073/pnas.1512878112
[Indexed for MEDLINE]
Free PMC Article

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