Short-term forms of presynaptic plasticity

Synapses exhibit several forms of short-term plasticity that play a multitude of computational roles. Short-term depression suppresses neurotransmitter release for hundreds of milliseconds to tens of seconds; facilitation and post-tetanic potentiation lead to synaptic enhancement lasting hundreds of milliseconds to minutes. Recent advances have provided insight into the mechanisms underlying these forms of plasticity. Vesicle depletion, as well as inactivation of both release sites and calcium channels, contribute to synaptic depression. Mechanisms of short-term enhancement include calcium channel facilitation, local depletion of calcium buffers, increases in the probability of release downstream of calcium influx, altered vesicle pool properties, and increases in quantal size. Moreover, there is a growing appreciation of the heterogeneity of vesicles and release sites and how they can contribute to use-dependent plasticity.

► Synapses exhibit several forms of short-term plasticity. ► Depression is due to vesicle depletion as well as release site and calcium channel inactivation. ► Residual calcium, calcium channel facilitation, and buffer saturation underlie facilitation. ► PTP results from an increase in release probability, but other mechanisms have also been proposed. ► Heterogenous vesicular properties complicate interpretation of PTP mechanisms.