Updated 2 months, 2 weeks ago

Sleep deprivation handicaps the brain's ability to form new memories

Studying mice, scientists at Johns Hopkins have fortified evidence that a key purpose of sleep is to recalibrate the brain cells responsible for learning and memory so the animals can “solidify” lessons learned and use them when they awaken in the case of nocturnal mice, the next evening.

Scientists believe memories are encoded through these synaptic changes. But there’s a hitch in this thinking, Diering says, because while mice and other mammals are awake, the synapses throughout its brain tend to be strengthened, not weakened, pushing the system toward its maximum load. When neurons are “maxed out” and constantly firing, they lose their capacity to convey information, stymying learning and memory.

One possible reason that neurons don't usually max out is a process that has been well-studied in lab-grown neurons but not in living animals, asleep or awake.

Known as homeostatic scaling down, it is a process that uniformly weakens synapses in a neural network by a small percentage, leaving their relative strengths intact and allowing learning and memory formation to continue.

To learn specifically which molecules were responsible for the phenomenon, the team turned to a protein called Homer1a, discovered in 1997 by Paul Worley, professor of neuroscience, who was also part of the team conducting the new study.

Studies showed that Homer1a; named for the ancient Greek author and the scientific “odyssey” required to identify it; is important for the regulation of sleep and wakefulness, and for homeostatic scaling down in lab-grown neurons.

As predicted, levels of Homer1a in the receiving synapses were much higher in the sleep-deprived mice than in those that got recovery sleep. That suggests, says Diering that Homer1a is sensitive to an animal's "sleep need," not just what time of day it is.

Graham Diering, Ph.D., the postdoctoral fellow who led the study, explained that the results from the mouse study can be used to make determinations about the human brain.

“Our findings solidly advance the idea that the mouse and presumably the human brain can only store so much information before it needs to recalibrate,” he said in a statement.

“Without sleep and the recalibration that goes on during sleep, memories are in danger of being lost.”

Among the events that require further exploration is how learning and memory are affected by sleep disorders and other diseases known to disrupt sleep in humans, like Alzheimer's disease and autism.

Huganir also says that benzodiazapines and other drugs that are commonly prescribed as sedatives, such as muscle relaxants and other sleep aids, are known to prevent homeostatic scaling down and are likely to interfere with learning and memory, though that idea has yet to be tested experimentally.

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