Blockade of GluN2B-Containing NMDA Receptors Prevents Potentiation and Depression of Responses during Ocular Dominance Plasticity

J Neurosci. 2024 Sep 4;44(36):e0021232024. doi: 10.1523/JNEUROSCI.0021-23.2024.

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.

Keywords: GluN2B; LTP; NMDA; monocular deprivation; ocular dominance plasticity; visual cortex.

MeSH terms

  • Animals
  • Dominance, Ocular* / physiology
  • Evoked Potentials, Visual / physiology
  • Excitatory Amino Acid Antagonists / pharmacology
  • Excitatory Postsynaptic Potentials* / drug effects
  • Excitatory Postsynaptic Potentials* / physiology
  • Female
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology
  • Long-Term Synaptic Depression / drug effects
  • Long-Term Synaptic Depression / physiology
  • Male
  • Mice
  • Mice, Inbred C57BL*
  • Neuronal Plasticity* / drug effects
  • Neuronal Plasticity* / physiology
  • Photic Stimulation / methods
  • Receptors, N-Methyl-D-Aspartate* / antagonists & inhibitors
  • Receptors, N-Methyl-D-Aspartate* / metabolism
  • Sensory Deprivation / physiology
  • Visual Cortex / drug effects
  • Visual Cortex / physiology

Substances

  • Receptors, N-Methyl-D-Aspartate
  • NR2B NMDA receptor
  • Excitatory Amino Acid Antagonists