Blockade of GluN2B-Containing NMDA Receptors Prevents Potentiation and Depression of Responses during Ocular Dominance Plasticity
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Updated: Jun 17, 2025
Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
Published on: February 8, 2020
Michelle C D Bridi1, Su Hong1, Daniel Severin1
1Zanvyl Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218.
Abstract:
Monocular deprivation (MD) causes an initial decrease in synaptic responses to the deprived eye in juvenile mouse primary visual cortex (V1) through Hebbian long-term depression (LTD). This is followed by a homeostatic increase, which has been attributed either to synaptic scaling or to a slide threshold for Hebbian long-term potentiation (LTP) rather than scaling. We therefore asked in mice of all sexes whether the homeostatic increase during MD requires GluN2B-containing NMDA receptor activity, which is required to slide the plasticity threshold but not for synaptic scaling. Selective GluN2B blockade from 2-6 d after monocular lid suture prevented the homeostatic increase in miniature excitatory postsynaptic current (mEPSC) amplitude in monocular V1 of acute slices and prevented the increase in visually evoked responses in binocular V1 in vivo. The decrease in mEPSC amplitude and visually evoked responses during the first 2 d of MD also required GluN2B activity. Together, these results support the idea that GluN2B-containing NMDA receptors first play a role in LTD immediately following eye closure and then promote homeostasis during prolonged MD by sliding the plasticity threshold in favor of LTP.
Insights
Monocular deprivation (MD) in mice initially reduces visual cortex responses via LTD, then increases them. GluN2B-NMDA receptor activity is crucial for both the initial decrease and the later homeostatic increase during prolonged MD.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Visual System Development
Background:
- Monocular deprivation (MD) in juvenile mice alters synaptic responses in the primary visual cortex (V1).
- The homeostatic increase following initial response decrease is debated, attributed to synaptic scaling or plasticity threshold shifts.
- GluN2B-containing NMDA receptors are implicated in plasticity threshold shifts but not synaptic scaling.
Purpose of the Study:
- To investigate the role of GluN2B-containing NMDA receptors in the homeostatic increase of synaptic responses during prolonged monocular deprivation.
- To determine if GluN2B activity is required for both the initial decrease and subsequent increase in visual cortex synaptic function.
Main Methods:
- Utilized selective GluN2B blockade in juvenile mice of all sexes.
- Measured miniature excitatory postsynaptic current (mEPSC) amplitude in acute V1 slices.
- Assessed visually evoked responses in V1 in vivo using electrophysiology.
Main Results:
- Selective GluN2B blockade prevented the homeostatic increase in mEPSC amplitude during prolonged MD.
- GluN2B blockade also prevented the increase in visually evoked responses in vivo.
- The initial decrease in mEPSC amplitude and visually evoked responses during the first 2 days of MD also required GluN2B activity.
Conclusions:
- GluN2B-containing NMDA receptors are essential for the initial decrease in synaptic responses following eye closure.
- These receptors play a critical role in promoting homeostasis during prolonged MD by facilitating LTP via plasticity threshold sliding.
- The findings support a dual role for GluN2B in regulating synaptic plasticity during visual system development under deprivation conditions.
