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The Neuroscientist Comments

One of the catechisms of contemporary neuroscience is that learning involves selective modifications in synaptic efficacy. Much of what we understand about synaptic mechanisms associated with learning has been derived from studies on long-term potentiation, and it has been suggested that the synaptic strengthening that occurs during LTP involves the addition of GluR1 subunit–containing AMPA-type glutamate receptors. Now Rumpel and associates (2005), using auditory fear conditioning, have tested the hypothesis that a learningdriven increase in GluR1 receptors at selective synapses underlies associative memory. Building on the putative role of the amygdala in acquisition and storage of fear memory traces, these investigators studied the role of GluR1-receptor trafficking at thalamo-amygdala synapses in associative fear conditioning. Using amplicon vectors to monitor and perturb AMPA receptor trafficking, these investigators first observed that there was little or no synaptic incorporation of GluR1 receptors within the lateral amygdala of naive rats. Next, they tested a key predication of the receptor trafficking hypothesis, that is, that conditioning should induce the incorporation of GluR1 receptors into thalamo-amygdala synapses, and they observed that associative fear conditioning is a powerful stimulus for incorporation of these receptors into synapses within the lateral amygdala that receives auditory input. Building on these results, they next demonstrated that receptor trafficking induced by fear conditioning is not a generalized or global phenomenon but is rather restricted to a subset of synapses. Rumpel and associates next tested another predication of the trafficking hypothesis, that is, that synaptic delivery of endogenous GluR1 receptors is a prerequisite for acquisition of the condition response, and they observed that blockade of synaptic GluR1-receptor incorporation within the lateral amygdala disrupts the learning process underlying the lasting form of associative memory. Finally, these authors estimated the fraction of neurons with the lateral amygdala that must exhibit plasticity for fear conditioning to occur, and they found that memory was reduced if AMPA receptor synaptic incorporation was blocked in as few as 10% to 20% of neurons within the lateral amygdala. On the basis of these studies, the authors concluded that the encoding of memories within the lateral amygdala is mediated by AMPA receptor trafficking, is broadly distributed, and displays little redundancy. Future studies will undoubtedly focus on the question of whether these conclusions apply to other areas of the brain.