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One of the most intriguing features of the brain is its ability not only to process and acquire information about the external world through learning but also to store it for posterity as memory. The prevailing view is that learning occurs via experience-dependent changes in the electrical properties of ensembles of neurons. Memory is the maintenance of that altered state of neuronal activity.
Synaptic plasticity, the change in synaptic efficacy in response to external cues, can change the electrical properties of ensembles of neurons and thus is believed to be one of the cellular mechanisms of memory storage. The long-term changes in synaptic efficacy are at least partly due to activity-dependent changes in the molecular composition of the synapses, which is accompanied by the structural alteration of preexisting synapses and growth of new synapses. However, if a change in synaptic efficacy is indeed the underlying mechanism of memory storage, then the experience-dependent molecular changes of the synapse as well as the structural changes must be maintained for the duration of the memory.
If this were true, it raises the following questions: 1) How do external cues alter the molecular composition of the synapse? 2) What is the nature of this altered molecular composition? 3) Since the biological molecules have a relatively short half-life (hours to days) compared to the duration of memory (years), how is the altered molecular composition of a synapse maintained for such a long time, if it is maintained?
Our lab is focused on understanding these questions using marine snail Aplysia and fruit fly Drosophila as model organisms.
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