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Sensory experience drives plasticity of the body map in developing and adult somatosensory cortex, but the synaptic mechanisms underlying such plasticity are not well understood. Recently, several mechanisms that are likely to contribute to map plasticity have been directly observed in response to altered experience in vivo. These mechanisms include long-term potentiation and long-term depression at specific excitatory synapses, competition between lemniscal (barrel) and non-lemniscal (septal) processing streams, and regulation of the number of inhibitory synapses. [Copyright &y& Elsevier]

Physiological roles for postsynaptic molecules in synaptogenesis and plasticity are under intense investigation. Recent imaging experiments, including GFP-based and single-particle tracking strategies, reveal rapid movement of synaptic components to and from the postsynaptic sites. Furthermore, specific patterns of neuronal activity and/or activation of specific transmitter receptors trigger selective translocation of postsynaptic components. These emerging dynamic properties of synaptic specializations add another layer of complexity to the signaling mechanisms of CNS synapses. [Copyright &y& Elsevier]

Although the strength of quantal synaptic transmission is jointly controlled by pre- and post-synaptic mechanisms, the presynaptic mechanisms remain substantially less well characterized. Recent studies reveal that a single package of neurotransmitter is generally insufficient to activate all available postsynaptic receptors, whereas the sum of transmitter from multiple vesicles can result in receptor saturation. Thus, depending upon the number of vesicles released, a given synaptic pathway might be either ‘reliable’ or ‘unreliable’. A lack of receptor saturation in turn makes it possible to modify quantal size by altering the flux of transmitter through the synaptic cleft. Studies are now illuminating several new mechanisms behind the regulation of this transmitter flux — characteristics that control how transmitter is loaded into vesicles, how it is released and the manner by which it interacts with postsynaptic receptors. [Copyright &y& Elsevier]