Marcos Frank, PhD, Assistant Professor of Neuroscience, at the University of Pennsylvania School of Medicine, along with postdoctoral researcher Sara Aton, PhD, and colleagues have shown that the functions associated with long-term memory formation don’t become active until we sleep.
In a cleverly designed series of experiments, the researchers worked with the visual systems of young animals. By covering one eye of the animals with a patch the team studied the electrophysiological and molecular changes that resulted with or without sleep (and compared these to a control group with no patch).
Once triggered to reorganize its neural networks in wakefulness (by visual deprivation, for instance), the brain engages intra- and intercellular communication pathways, releasing a series of enzymes that could reorganize the appropriate neurons.
“To our amazement, we found that these enzymes never really turned on until the animal had a chance to sleep,” Dr. Frank explained, “As soon as the animal had a chance to sleep, we saw all the machinery of memory start to engage.”
(Further, by stopping these enzymes from working in the sleeping brain the normal reorganization of the cortex didn’t happen.)
But perhaps more generally interesting is the insight that the changes in some senses weren’t memory changes — although they were certainly plastic changes. The same mechanism could play a role in all neurological plasticity processes.