It is obvious that pulling a late
nighter when the objective is to put more information into memory is seriously
counter productive. A more appropriate
approach is to complete all memory oriented work during the six hours before
beginning a full night’s sleep. Then on
awakening, peruse a refresher sheet.
However one is prepared,
deviating from this approach will gain you nothing. The other lesson is that memorization needs
to be bracketed by sleep in order for the brain to do its work. Thus learning is a process of intense work
swapped with a sound sleep. Somehow we
probably did just that but forgot it along the way.
The other obvious take home is to
prepare for a class by reviewing the previous class just before going to
sleep. Make that part of your routine. Doing homework normally forces one to
actually do this, but that is not always possible.
The roots of memory impairment resulting from sleep deprivation
by Staff Writers
From high-school students to surgeons, anyone who has pulled an all-nighter knows there is a price to be paid the next day: trouble focusing, a fuzzy memory and other cognitive impairments. Now, researchers at Penn have found the part of the brain and the neurochemical basis for sleep deprivation's effects on memory.
Ted Abel, a professor of biology in Penn's School of Arts and Sciences
and director of the University's interdisciplinary Biological Basis of Behavior
program, led the research team. His partners included Cedrick Florian, a postdoctoral
fellow in biology, and Christopher Vecsey, a neuroscience graduate student, as
well as researchers from the Massachusetts Institute of Technology and Tufts University
Their research was published in The Journal of Neuroscience.
Abel's group aimed to better understand the role of the nucleoside
adenosine in the hippocampus, the part of the brain associated with memory
function.
"For a long time, researchers have known that sleep deprivation results
in increased levels of adenosine in the brain, and has this effect from fruit
flies to mice to humans." Abel said. "There is accumulating evidence
that this adenosine is really the source of a number of the deficits and impact
of sleep deprivation, including memory loss and attention deficits. One
thing that underscores that evidence is that caffeine is
a drug that blocks the effects of adenosine, so we sometimes refer to this as
'the Starbucks experiment.'"
Abel's research actually involved two parallel experiments on
sleep-deprived mice, designed to test adenosine's involvement in memory
impairment in different ways.
One experiment involved genetically engineered mice. These mice were
missing a gene involved in the production of glial transmitters, chemicals
signals that originate from glia, the brain cells that support the function of
neurons. Without these gliatransmitters, the engineered mice could not produce
the adenosine the researchers believed might cause the cognitive effects
associated sleep deprivation.
The other experiment involved a pharmacological approach. The
researchers grafted a pump into the brains of mice that hadn't been genetically
engineered; the pump delivered a drug that blocked a particular adenosine
receptor in the hippocampus. If the receptor was indeed involved in memory impairment,
sleep-deprived mice would behave as if the additional adenosine in their brains
was not there.
To see whether these mice showed the effects of sleep deprivation, the
researchers used an object recognition test. On the first day, mice were placed
in a box with two objects and were allowed to explore them while being
videotaped. That night, the researchers woke some of the mice halfway through
their normal 12-hour sleep schedule.
On the second day, the mice were placed back in the box, where one of
the two objects had been moved, and were once again videotaped as they explored
to see how they reacted to the change.
"Mice would normally explore that moved object more than other
objects, but, with sleep deprivation, they don't," Abel said. "They
literally don't know where things are around them."
Both sets of treated mice explored the moved object as if they had
received a full night's sleep.
"These mice don't realize they're sleep-deprived," Abel
said.
Abel and his colleagues also examined the hippocampi of the mice, using
electrical current to measure their synaptic plasticity, or how strong and
resilient their memory-forming synapses were. The pharmacologically and
genetically protected mice showed greater synaptic plasticity after being sleep
deprived than the untreated group.
Combined, the two experiments cover both halves of the chemical pathway
involved in sleep deprivation. The genetic engineering experiment shows where
the adenosine comes from: glia's release of adenosine triphosphate, or ATP, the
chemical by which cells transfer energy to one another. And the pharmacological
experiment shows where the adenosine goes: the A1 receptor in the hippocampus.
The knowledge that interrupting the pathway at either end results in
mice that show no memory impairments is a major step forward in understanding
how to manage those impairments in humans.
"To be able to reverse a particular aspect of sleep-deprivation,
such as its effect on memory storage, we really want to understand the
molecular pathways and targets," Abel said. "Here, we've identified
the molecule, the cellular circuit and the brain region by which sleep
deprivation affects memory storage."
Such treatments would be especially enticing, given how sensitive the
brain is to sleep deprivation's effects.
"Our sleep deprivation experiments are the equivalent of losing
half of a night sleep for a single night," Abel said. "Most of us
would think that's pretty minor, but it shows just how critical the need for
sleep is for things like cognition."
In addition to Abel, Florian and Vescey, the research was conducted by
Michael M. Halassa of the Department of Psychiatry at Massachusetts General Hospital
and the Department of Brain and Cognitive Science at MIT, as well as Philip G.
Haydon, of the Department of Neuroscience at the Tufts University School of
Medicine. The research was supported by the National Institutes of Health.
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