The shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

中文翻译：

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弱视的关键时期

由单眼剥夺引起的双眼神经元眼优势 (OD) 的转变是突触可塑性的典型模型，仅限于出生后的关键时期。对这种可塑性的发育限制不仅为成熟的视觉皮层电路提供了稳定性，而且还阻碍了从弱视中恢复到早期窗口之外的能力。利用分子、遗传和成像工具的力量的小鼠模型的进展开始揭示控制初级视觉皮层 (V1) 可塑性关键时期开始和结束的电路、细胞和分子机制。新出现的证据表明，促进青少年可塑性的机制不仅会随着年龄的增长而丧失，而是可塑性受到分子“刹车”的发育上调的积极限制。解除这些刹车可增强成人视觉皮层的可塑性，并可用于促进弱视的恢复。通过实验操作重新激活可塑性已经修正了强大的 OD 可塑性仅限于出生后早期发育的观点。在这里，我们讨论了最近对关键时期开始和终止的神经生物学的见解，以及我们对这些过程的日益机械化的理解如何用于改进成人弱视的临床治疗。