The dynamic capacity for synapses in the cerebral cortex to change their signaling efficiency is thought to underlie many aspects of learning and experience-dependent modification. The cellular and molecular processes that mediate activity-dependent synaptic plasticity including the visual cortex. Such activity-dependent changes in synaptic signaling in the visual cortex, whether of a transient or sustained nature also have been suggested to contribute to dynamic cortical processing of visual input with consequences for visual perception, cognitive performance, skill- learning and developmental re-organization and refinement of functional visual cortical synaptic networks. However, the developmental regulation of these forms of synaptic plasticity has received less attention. In the visual cortex, dramatic consequences of environmental rearing conditions, peripheral sensory deficits such as retinal lesions, strabismus or form vision disturbances have been demonstrated at the level of neuronal structure, function and behavior. We utilize a model of neocortical synaptic plasticity (the DCM model) to characterize the cellular processes that are responsible for a type of functional synaptic plasticity in the visual neo-cortex of mature and neonatal animals. We have previously found that this form of synaptic plasticity, or covariance-induced- potentiation (CIP), occurs in individual pyramidal neurons of the adult visual cortex and it is triggered by activation of the N-methyl-D aspartate (NMDA) glutamate receptors and a rise in postsynaptic intracellular calcium. The induction of CIP is considerably more robust in the neonatal versus the mature visual cortex. However, the cellular mechanism for triggering the synaptic potential undergoes a dramatic developmental switch. The triggering mechanism switches from an NMDA-receptor independent to an NMDA-receptor dependent process. We have posited a developmentally controlled alteration in the coupling mechanism between voltage detection by metabotropic glutamate receptors and voltage-gated calcium channels, respectively. We will identify the molecular coincidence detector and signaling cascade for this type of developmentally regulated plasticity by combining electrophysiological techniques with high-resolution calcium imaging.
