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Neuron. 2014 Aug 20;83(4):879-93. doi: 10.1016/j.neuron.2014.07.039.

Synapse-specific control of experience-dependent plasticity by presynaptic NMDA receptors.

Author information

1
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA.
2
UNC Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA.
3
Neurobiology Curriculum, University of North Carolina, Chapel Hill, NC 27599, USA.
4
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA; Neurobiology Curriculum, University of North Carolina, Chapel Hill, NC 27599, USA; UNC Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA; Carolina Institute for Developmental Disabilities, University of North Carolina, Chapel Hill, NC 27599, USA.
5
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA; Neurobiology Curriculum, University of North Carolina, Chapel Hill, NC 27599, USA; UNC Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA; Carolina Institute for Developmental Disabilities, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: bphilpot@med.unc.edu.

Erratum in

  • Neuron. 2014 Sep 17;83(6);1481.

Abstract

Sensory experience orchestrates the development of cortical circuitry by adaptively modifying neurotransmission and synaptic connectivity. However, the mechanisms underlying these experience-dependent modifications remain elusive. Here we demonstrate that visual experience suppresses a presynaptic NMDA receptor (preNMDAR)-mediated form of timing-dependent long-term depression (tLTD) at visual cortex layer (L) 4-2/3 synapses. This tLTD can be maintained during development, or reinstated in adulthood, by sensory deprivation. The changes in tLTD are mirrored by changes in glutamate release; visual deprivation enhances both tLTD and glutamate release. These effects require the GluN3A NMDAR subunit, the levels of which are increased by visual deprivation. Further, by coupling the pathway-specific optogenetic induction of tLTD with cell-type-specific NMDAR deletion, we find that visual experience modifies preNMDAR-mediated plasticity specifically at L4-L2/3 synapses.

PMID:
25144876
PMCID:
PMC4181612
DOI:
10.1016/j.neuron.2014.07.039
[Indexed for MEDLINE]
Free PMC Article

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