Summary

Fast point-to-point communication between neurons in the brain is mediated by chemical synaptic transmission. During brief trains of action potentials (APs) in a presynaptic neuron, the response in the postsynaptic cell will not follow with equal strength. Rather, processes of short-term plasticity will decrease the amplitude of postsynaptic potentials (PSPs) during short-term depression, or increase PSP amplitudes, as occurs during shortterm enhancement (STE) of synaptic transmission. Various phases of STE can be distinguished based on their kinetics of decay after brief trains of presynaptic activity: Facilitation, augmentation and posttetanic potentiation. STE of synaptic transmission is induced by a rise of Ca2+ in presynaptic nerve terminals, and represents an increased number of vesicles which fuse in response to a presynaptic AP. Facilitation, which decays within less than half a second, is the shortest form of Ca2+-induced plasticity identified so far. STE and synaptic depression can be expressed simultaneously at a synapse, but the degree, and the direction of short-term plasticity is specifically regulated at a given type of synapse, and subject to modulation during postnatal development. This chapter discusses the presynaptic, Ca2+-dependent mechanisms of STE of synaptic transmission.

Overview of chemical synaptic transmission

Synaptic transmission takes place at specialized contact sites, at which the active zone of the presynaptic neuron approaches the postsynaptic density of a postsynaptic neuron (Fig. 3.1). Transmission is initiated when an action potential (AP) arrives at the nerve terminal, where it opens voltage-gated Ca2+ channels.