Short-term plasticity · Grey Matter

Short-term plasticity is the change in a synapse's strength from one spike to the next during a train, lasting from milliseconds to minutes, and it makes every synapse a small filter that responds differently to a single spike, a burst or a steady stream.

Short-term plasticity. Short-term plasticity is the change in a synapse's strength from one spike to the next during a train, lasting from milliseconds to minutes, and it makes every synapse a small filter that responds differently to a single spike, a burst or a steady stream.

Two opposite effects compete at the presynaptic terminal. Facilitation is growth of the response when spikes come close together: calcium left over from one spike (residual calcium) adds to the calcium of the next and raises its release probability, over tens to hundreds of milliseconds. Depression is the shrinking of the response during a train: each spike uses up some of the readily releasable vesicles, and if they are not replaced in time, later spikes find fewer ready to go. Which one wins depends mostly on the starting release probability: synapses that release a lot at the first spike deplete and depress, synapses that rarely release at first facilitate.

Each synapse has a character. Depressing synapses respond best to the onset of activity and to changes; facilitating ones respond best to sustained bursts.

The effects are presynaptic and temporary. Nothing is learned; the synapse returns to baseline within seconds or minutes, unlike long-term potentiation.

Longer-lasting forms exist. Augmentation and post-tetanic potentiation, after long high-frequency trains, last seconds to minutes and also come from accumulated calcium in the terminal.

Short-term plasticity makes a synapse care about rhythm.

The same average firing rate delivers different messages depending on whether the spikes arrive spread out or in bursts.

Questions: Why do some synapses grow stronger during a burst while others grow weaker? It depends mostly on how likely the synapse is to release at the first spike. A synapse with a low release probability keeps most of its ready vesicles, and the calcium left over from each spike adds to the next, so release grows during the burst (facilitation); a slow, high-affinity calcium sensor, synaptotagmin-7, contributes to this at many synapses. A synapse with a high release probability spends its ready vesicles on the first spikes and cannot refill them fast enough, so release shrinks (depression). The same presynaptic train therefore reaches one target as a growing signal and another as a fading one. What are the vesicle pools, and what happens when the ready one runs out? A terminal's vesicles fall into three functional groups: a readily releasable pool docked and primed at the active zone (about 1 to 2 % of the total), a recycling pool that refills it during normal activity (about 5 to 20 %), and a reserve pool holding most of the rest, mobilised only by intense stimulation. During a fast train each spike spends some of the ready vesicles, and if refilling cannot keep up, later spikes release less, which is short-term depression. Recovery takes from hundreds of milliseconds to seconds, depending on how quickly vesicles are recycled and primed again. How large the ready pool is, and how fast it refills, sets how long a synapse can follow a high-frequency input.