Chapter 17 Developmental mechanisms for regulating signal amplification at excitatory synapses in the neocortex

Abstract

Publisher Summary Sensory cortical areas exhibit a profound sensitivity to manipulation of inputs during the critical periods of development. The visual system is a classic example where profound structural and functional changes occur in synaptic circuits in response to imbalances in patterned input from the eyes. Although the sensitivity to various forms of sensory manipulation is greatest during particular critical periods of postnatal development, the cerebral cortex remains capable of a variety of profound alterations in its functional architecture well into adulthood. During the critical periods of postnatal development, there is evidence that major neuroanatomical reorganization contributes to the plasticity. In the adult cortex, the dynamic capacity for functional reorganization appears to be largely a function of variable synaptic efficiency. A particular synaptic covariance model (the Bienenstock, Cooper and Munro [BCM] model) has been successful in describing rules for transient changes in synaptic weights in visual cortex. N-methyl-D-aspartate (NMDA) receptors are critical for induction of covariance-induced synaptic potentiation and nitric oxide (NO) play a role in the process in the adult but not the immature cortex. Long-term synaptic depression is also developmentally regulated and shows a layer-specific maturational gradient that is revealed when excitatory synaptic transmission is studied in isolation from postsynaptic inhibition. A causal linkage between short-term modifications in synaptic efficiency and longer term changes in anatomical connections, such as ocular dominance column plasticity is still circumstantial and awaits experimental validation. N-methyl-D-aspartate receptor (NMDAR)-mediated NO production is a viable process in the mature cortex.