Various forms of synaptic plasticity underlie aspects of learning and memory. Synaptic augmentation is a form of short-term plasticity characterized by synaptic enhancement that persists for seconds following specific patterns of stimulation. The mechanisms underlying this form of plasticity are unclear but are thought to involve residual presynaptic Ca²⁺. Here, we report that augmentation was reduced in cultured mouse hippocampal neurons lacking the Ca²⁺ sensor, Doc2; other forms of short-term enhancement were unaffected. Doc2 binds Ca²⁺ and munc13 and translocates to the plasma membrane to drive augmentation. The underlying mechanism was not associated with changes in readily releasable pool size or Ca²⁺ dynamics, but rather resulted from superpriming a subset of synaptic vesicles. Hence, Doc2 forms part of the Ca²⁺-sensing apparatus for synaptic augmentation via a mechanism that is molecularly distinct from other forms of short-term plasticity.

各种形式的突触可塑性是学习和记忆的基础。突触增强是一种短期可塑性，其特征在于突触增强在特定刺激模式下持续数秒。这种可塑性的潜在机制尚不清楚，但被认为与残余突触前Ca ^2+有关。在这里，我们报告说，缺少Ca ²⁺传感器Doc2的培养的小鼠海马神经元的扩增减少。其他形式的短期增强不受影响。Doc2结合Ca ²⁺和munc13并转运至质膜以驱动扩增。潜在的机制与易于释放的池大小或Ca ^2+的变化无关动力学，而是由超灌注突触小泡的子集引起的。因此，Doc2通过分子机制不同于其他形式的短期可塑性的机制，构成了用于突触增强的Ca ²⁺传感设备的一部分。