Doc2-mediated superpriming supports synaptic augmentation

Significance Plastic changes in synaptic connections constitute the basis of learning and memory. Different forms of synaptic plasticity are generally distinguished experimentally by their timescales, but it is unclear whether each form of plasticity corresponds to a distinct biological process with a dedicated molecular mechanism. In the present study, we show that the Ca2+ -binding protein, Doc2, “superprimes” a subset of already primed synaptic vesicles to make them more likely to release, and this process selectively contributes to augmentation (on the scale of seconds). The underlying molecular mechanism does not mediate other forms of short-term enhancement (that occur on the timescale of milliseconds or minutes). This work establishes a function of Doc2 in maintaining synaptic plasticity within a narrow time window.