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.

单眼剥夺 （MD） 导致幼年小鼠初级视觉皮层 （V1） 到 Hebbian 长期抑郁 （LTD） 对剥夺眼的突触反应最初降低。随后是稳态增加，这归因于突触缩放或 Hebbian 长期增强 （LTP） 的滑动阈值，而不是缩放。因此，我们在所有性别的小鼠中询问 MD 期间稳态增加是否需要含有 GluN2B 的 NMDA 受体活性，这是滑动可塑性阈值所必需的，但不是突触缩放所必需的。单眼睑缝合后 2-6 d 选择性阻断 GluN2B 阻止了急性切片单眼 V1 中微型兴奋性突触后电流 （mEPSC） 振幅的稳态增加，并阻止了体内双眼 V1 视觉诱发反应的增加 MD 前 2 d 期间 mEPSC 振幅和视觉诱发反应的降低也需要 GluN2B 活性。总之，这些结果支持这样一种观点，即含 GluN2B 的 NMDA 受体在闭眼后立即在 LTD 中发挥作用，然后通过滑动可塑性阈值以支持 LTP 来促进延长 MD 期间的稳态。