Postsynaptic receptor mechanisms underlying developmental speeding of synaptic transmission

As animals mature the decay of postsynaptic currents become faster at a variety of synapses. This change is thought to contribute to a refinement of motor co-ordination and to an increase in the precision of sensory perception and cognition. At cholinergic neuromuscular synapses and glycinergic and GABAergic inhibitory synapses, the developmental speeding of synaptic currents depends upon switches of receptor subunits and an ensuing acceleration in the kinetics of channel gating. At glutamatergic excitatory synapses, speeding in the decay time of NMDA receptor (NMDAR)-mediated excitatory postsynaptic currents (NMDA-EPSCs) is also dependent on developmental switches in NMDAR subunits. However, developmental speeding in the kinetics of AMPA receptor (AMPAR)-mediated EPSCs (AMPA-EPSCs) is caused by multiple factors. The decay time of AMPA-EPSCs can be shaped by the kinetics of channel gating or desensitization of AMPA receptors, depending upon the speed of transmitter clearance from the synaptic cleft. During postnatal development AMPAR channel gating and desensitization as well as the transmitter clearance speed up in kinetics. Given that the developmental speeding of synaptic currents play critical roles in the maturation of sensory and motor functions, any defect in this mechanism may seriously affect neuronal function.