Neuron
Volume 83, Issue 4, 20 August 2014, Pages 879-893
Journal home page for Neuron

Article
Synapse-Specific Control of Experience-Dependent Plasticity by Presynaptic NMDA Receptors

https://doi.org/10.1016/j.neuron.2014.07.039Get rights and content
Under an Elsevier user license
open archive

Highlights

  • Visual deprivation in adulthood promotes presynaptic L4-L2/3 tLTD

  • Deprivation increases the contribution of preNMDARs to glutamate release and tLTD

  • Visual experience regulates the GluN3A NMDAR subunit, which is required for tLTD

  • Sensory experience regulates tLTD in a synapse-specific manner

Summary

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.

Cited by (0)

5

Present address: Allen Institute for Brain Science, Seattle, WA 98103, USA

6

Present address: Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA