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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]

Neuronal responses to electrical activity-induced calcium signals are specified by the localization of the calcium entry site and the spatial properties of the calcium transient. Calcium flux through NMDA receptors located in the synapse initiates changes in synaptic efficacy and promotes pro-survival events, whereas calcium flux through extrasynaptic NMDA receptors is coupled to cell death pathways. The dialogue between the synaptic NMDA receptors and the nucleus is also modulated by extrasynaptic NMDA receptors, which shut down activity of CRE-binding protein (CREB) and antagonize the increase in brain-derived neurotrophic factor (BDNF) expression induced by synaptic NMDA receptors. The specification of the biological response by the localization of the receptor activated is a new concept in neuronal calcium signalling that can explain many of the opposing roles of NMDA receptors. [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]

The ability to learn novel motor skills has fundamental importance for adaptive behavior. Neocortical mechanisms support human motor skill learning, from simple practice to adaptation and arbitrary sensory–motor associations. Behavioral and neural manifestations of motor learning evolve in time and involve multiple structures across the neocortex. Modifications of neural properties, synchrony and synaptic efficacy are all related to the development and maintenance of motor skill. [Copyright &y& Elsevier]