Abstract
The requirement for transcription during long-lasting forms of learning-related synaptic plasticity raises the question of how the products of gene expression can be targeted to alter synaptic strength at some but not all synapses made by a neuron. The synaptic tagging hypothesis proposes that the products of gene expression are delivered throughout the cell, but they only function to increase synaptic strength when they are ‘captured’ at specific synapses that have been ‘tagged’ by previous synaptic activity. Studies in a variety of systems have confirmed the existence of synaptic tagging and capture, and current research is aimed at identifying the molecular nature of the tag.
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