Feeling Lost? Get More
Sleep
Losing sleep may undo the rejuvenating
effects of new learning on the brain; Ironically, lack of sleep may improve
performance on some tasks
BETHESDA, Md. (Jan. 6, 2006) – As the pace of life
quickens and it becomes harder to balance home and work, many people meet
their obligations by getting less sleep.
But sleep deprivation impairs spatial learning --
including remembering how to get to a new destination. And now scientists
are beginning to understand how that happens: Learning spatial tasks
increases the production of new cells in an area of the brain involved with
spatial memory called the hippocampus. Sleep plays a part in helping those
new brain cells survive.
A team of researchers from the University of California
and Stanford University found that sleep-restricted rats had a harder time
remembering a path through a maze compared to their rested counterparts. And
unlike the rats that got enough sleep, the sleep-restricted rats showed
reduced survival rate of new hippocampus cells.
The researchers used sleep-restricted rats rather than
sleep-deprived rats to more closely mimic the common human experience of
inadequate sleep during the work week, said lead investigator Ilana Hairston
of both the University of California, Berkeley, and Stanford University. The
paper, “Sleep restriction suppresses neurogenesis induced by
hippocampus-dependent learning,” appears in the Journal of
Neurophysiology published by the American Physiological Society.
Stanford researchers Milton T.M. Little, Michael D. Scanlon, Monique T.
Barakat, Theo D. Palmer, Robert M. Sapolsky, and H. Craig Heller co-authored
the paper.
Learning appears to
rejuvenate the brain
Scientists already know – and most of us can confirm
from firsthand experience -- that lack of sleep impairs cognitive function.
Sleep-restricted individuals have a shorter attention span, impaired memory,
and a longer reaction time. “Sleep is necessary for general health, but it
now appears that the brain needs sleep more than any other part of the
body,” Hairston said.
Previous studies have shown that the hippocampus is
important for spatial learning. “The hippocampus also has the unique ability
to generate new brain cells throughout life, a process called ‘neurogenesis,’”
Hairston noted. “When animals learn a task that requires the hippocampus,
the rate of neurogenesis increases. This suggests that learning itself
rejuvenates the brain.”
Knowing that spatial learning triggers production of
new brain cells in the hippocampus, Hairston and her team wanted to find out
whether restricting sleep during a spatial learning task would affect new
cell production in the hippocampus.
The experiment: swimming
to the exit platform
The researchers trained rats on one of two tasks using
a water maze -- a plastic pool about six feet in circumference and two feet
deep. Rats were placed in the water and had to swim to the exit platform.
One group could not see the platform, which was placed
underwater, and had to form a “mental map” of the maze -- a spatial memory
task that is hippocampus-dependent -- to quickly reach the exit.
The second group could see and smell the exit platform,
which had a citrus odor. The researchers moved the platform every fourth
trial, requiring the animal to rely on its senses, not on memory, to find
it. This task did not engage the hippocampus because the rat did not need a
mental map of the pool to reach the platform, Hairston explained.
Fewer brain cells for the
weary
At the end of each training session, half the animals
in each group were kept awake for six hours by being presented novel stimuli
that kept them interested and awake. The other half were returned to their
cages and allowed to sleep. After six hours, the sleep-restricted rats were
allowed to sleep for the remainder of the day until the next session, 18
hours later.
Rested animals that had to rely on memory to find the
goal showed increased neurogenesis in the hippocampus compared with animals
that could use sight and smell. That made sense, because the task that
relied on memory involved the hippocampus, while the other did not.
However, the sleep-restricted rats that had to rely on
memory to find the goal showed no increased neurogenesis, unlike their
rested counterparts. This means that lack of sleep undoes the cell
rejuvenation benefit that would normally come from the task, the researchers
noted.
Sleep restriction prompts
use of a secondary strategy
On the other hand, the sleep-restricted rats that were
required to locate the platform using visual and odor cues did better on the
task than their rested counterparts. This was an unexpected finding.
Hairston et al. believe it is because the rested group
tried to rely on memory to find the platform, generally a better strategy to
reach a goal you have reached before. But in this case, where the
researchers moved the goal every fourth trial, using the visual and odor
cues was a better strategy. It appears that the sleep-restricted rats
changed their strategy to compensate for their lack of sleep – and it
worked.
“The sleep-restricted rats in this group actually did
better because the lack of sleep interfered with their ability to memorize
the maze -- forcing them to rely on easily accessible cues,” Hairston said.
Researchers point to practical implications for the
overtired
Overall, the study underlined that learning depends
upon two things: exposure to novel material and getting a good night’s
sleep, Hairston said.
Learning new things, at least in the case of spatial
memory, quite literally keeps your brain young by ensuring a better survival
rate for new brain cells in the hippocampus. However, not getting enough
sleep eliminates the potential benefit of new learning on the hippocampus by
suppressing neurogenesis. “Mild, chronic sleep restriction may have
long-term deleterious effects on neural functioning,” according to the
paper.
On the other hand, that sleep-deprived rats did better
on a task requiring use of visual and odor cues compared to their better
rested counterparts “implies that some kinds of cognitive function are
resistant to sleep loss,” Hairston said. “This may be significant in human
learning as well, and implies that it may be possible to optimize the way
information is presented to rested versus fatigued individuals to take
advantage of the specific neural substrates that are unaffected by sleep
loss,” the researchers concluded.
“This finding could be used to design training regimens
for chronically sleep-deprived people, including members of the military and
medical students,” Hairston said. “That said, while the cognitive impairment
may be overcome, our findings indicate that mild, chronic sleep restriction
may have long-term deleterious effects on neural function,” according to the
paper.
Further studies could
clarify learning strategies the brain employs
One implication of these findings is that sleep
restriction disrupts the hierarchy of cognitive processes. That is, spatial
learning seemed to be the primary cognitive strategy, and only when it was
disrupted by lack of sleep, did a secondary strategy emerge. “It would be
interesting to expand our findings to see if other competing processes are
similarly affected by sleep restriction,” Hairston said.
For example, scientists know that people who have
suffered certain types of brain lesions may be unable to screen out
irrelevant stimuli such as random noises in a room, something healthy
individuals do easily. A flip side is that people with these lesions tend to
associate familiar stimuli with new information more rapidly than healthy
counterparts, a phenomenon called attention switching.
This suggests that learning to ignore stimuli and rapid
attention switching are competing processes, with healthy individuals
ignoring familiar stimuli as their primary strategy. It would be interesting
to assess whether sleep restriction causes people to lose the ability to
screen out extraneous stimuli and preferentially apply attention switching,
she said.
Source and funding
The paper “Sleep restriction suppresses neurogenesis
induced by hippocampus-dependent learning,” appears in the Journal of
Neurophysiology published by the American Physiological Society.
The research was done by Ilana S. Hairston at both the Psychology Department
of University of California, Berkeley, and the Department of Biological
Sciences of Stanford University, Palo Alto, California, and Milton T. M.
Little, Michael D. Scanlon, Monique T. Barakat, Robert M. Sapolsky, and H.
Craig Heller, of the Department of Biological Sciences of Stanford, and Theo
D. Palmer, at the Department of Neurosurgery at Stanford.
The research was funded by NIH and a pre-doctoral
National Institute of Mental Health award (Hairston).
Editor’s note: The media may obtain a copy of
Hairston et al. by contacting Christine Guilfoy, American Physiological
Society, (301) 634-7253, (978) 290-2400 (cell), or
cguilfoy@the-aps.org.
* * *
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