Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1. We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity. We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells. We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity.

中文翻译：

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经验依赖性视觉皮层可塑性中 NMDA 受体的独特层流要求。

初级视觉皮层（V1）是多种形式的依赖于经验的可塑性的所在地。一次限制对一只眼睛的视觉刺激表明，许多此类形式的可塑性是眼睛特异性的，这表明突触修饰发生在丘脑皮质输入的双眼整合之前。这些形式的可塑性的一个共同特征是需要 V1 中的 NMDA 受体 (NMDAR) 激活。因此，我们假设皮质层 4 (L4) 中的 NMDAR 接收最密集的丘脑皮质输入，对于所有形式的 NMDAR 依赖性和输入特异性 V1 可塑性都是必要的。我们在清醒的小鼠中测试了这一假设，使用遗传方法选择性地从 L4 主细胞中删除 NMDAR。我们出乎意料地发现，在没有 L4 NMDAR 的情况下，刺激选择性反应增强和单眼剥夺 (MD) 后的睁眼反应增强都会持续存在。相比之下，在缺乏 L4 NMDAR 的小鼠中，MD 驱动的剥夺眼反应的抑制受到损害，V1 切片中的 L4 长期抑制也受到损害。我们的研究结果揭示了 L4 NMDAR 在视觉皮质突触抑制中的关键需求，而它们在皮质反应增强中的作用却令人惊讶地可以忽略不计。这些结果表明，不同细胞亚群内的 NMDAR 支持不同形式的经验依赖性可塑性。