Context-dependent, dynamic changes in the size of receptive fields in the visual cortex can be induced by specific patterns of visual activity. Several pieces of evidence suggest that NMDA receptor-dependent, long-term synaptic plasticity might generate this effect, but to date the synaptic mechanisms ultimately responsible for the changes in receptive field size are unknown. We will determine if NMDA receptor-dependent synaptic plasticity underlies the plasticity in receptive field size. The questions we will specifically address are: 1) Do pharmacological manipulations that block NMDA receptor-dependent synaptic plasticity in visual cortex also block changes in receptive field size? 2) Do changes in receptive field size require coincident pre- and post-synaptic activity (which is required to activate NMDA receptors), and if so, are the temporal limits of this coincidence comparable to those required to induce NMDA receptor-dependent plasticity? This research will further our understanding of the rules by which synaptic activity affects sensory processing. An understanding of these rules is essential for a rational strategy to fix defects in visual processing associated with visual loss in degenerative eye disorders or damage to the eye.
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