It is obvious that pulling a latenighter when the objective is to put more information into memory is seriouslycounter productive. A more appropriateapproach is to complete all memory oriented work during the six hours beforebeginning a full night’s sleep. Then onawakening, peruse a refresher sheet.
However one is prepared,deviating from this approach will gain you nothing. The other lesson is that memorization needsto be bracketed by sleep in order for the brain to do its work. Thus learning is a process of intense workswapped with a sound sleep. Somehow weprobably did just that but forgot it along the way.
The other obvious take home is toprepare for a class by reviewing the previous class just before going tosleep. Make that part of your routine. Doing homework normally forces one toactually 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-nighterknows there is a price to be paid the next day: trouble focusing, a fuzzymemory and other cognitive impairments. Now, researchers at Penn have found thepart of the brain and the neurochemical basis for sleep deprivation's effectson memory.
Ted Abel, a professor of biology in Penn's School of Arts and Sciencesand director of the University's interdisciplinary Biological Basis of Behaviorprogram, led the research team. His partners included Cedrick Florian, a postdoctoralfellow in biology, and Christopher Vecsey, a neuroscience graduate student, aswell 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 nucleosideadenosine in the hippocampus, the part of the brain associated with memoryfunction.
"For a long time, researchers have known that sleep deprivation resultsin increased levels of adenosine in the brain, and has this effect from fruitflies to mice to humans." Abel said. "There is accumulating evidencethat this adenosine is really the source of a number of the deficits and impactof sleep deprivation, including memory loss and attention deficits. Onething that underscores that evidence is that caffeine isa 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 onsleep-deprived mice, designed to test adenosine's involvement in memoryimpairment in different ways.
One experiment involved genetically engineered mice. These mice weremissing a gene involved in the production of glial transmitters, chemicalssignals that originate from glia, the brain cells that support the function ofneurons. Without these gliatransmitters, the engineered mice could not producethe adenosine the researchers believed might cause the cognitive effectsassociated sleep deprivation.
The other experiment involved a pharmacological approach. Theresearchers grafted a pump into the brains of mice that hadn't been geneticallyengineered; the pump delivered a drug that blocked a particular adenosinereceptor in the hippocampus. If the receptor was indeed involved in memory impairment,sleep-deprived mice would behave as if the additional adenosine in their brainswas not there.
To see whether these mice showed the effects of sleep deprivation, theresearchers used an object recognition test. On the first day, mice were placedin a box with two objects and were allowed to explore them while beingvideotaped. That night, the researchers woke some of the mice halfway throughtheir normal 12-hour sleep schedule.
On the second day, the mice were placed back in the box, where one ofthe two objects had been moved, and were once again videotaped as they exploredto see how they reacted to the change.
"Mice would normally explore that moved object more than otherobjects, but, with sleep deprivation, they don't," Abel said. "Theyliterally don't know where things are around them."
Both sets of treated mice explored the moved object as if they hadreceived a full night's sleep.
"These mice don't realize they're sleep-deprived," Abelsaid.
Abel and his colleagues also examined the hippocampi of the mice, usingelectrical current to measure their synaptic plasticity, or how strong andresilient their memory-forming synapses were. The pharmacologically andgenetically protected mice showed greater synaptic plasticity after being sleepdeprived than the untreated group.
Combined, the two experiments cover both halves of the chemical pathwayinvolved in sleep deprivation. The genetic engineering experiment shows wherethe adenosine comes from: glia's release of adenosine triphosphate, or ATP, thechemical by which cells transfer energy to one another. And the pharmacologicalexperiment shows where the adenosine goes: the A1 receptor in the hippocampus.
The knowledge that interrupting the pathway at either end results inmice that show no memory impairments is a major step forward in understandinghow 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 themolecular pathways and targets," Abel said. "Here, we've identifiedthe molecule, the cellular circuit and the brain region by which sleepdeprivation affects memory storage."
Such treatments would be especially enticing, given how sensitive thebrain is to sleep deprivation's effects.
"Our sleep deprivation experiments are the equivalent of losinghalf of a night sleep for a single night," Abel said. "Most of uswould think that's pretty minor, but it shows just how critical the need forsleep is for things like cognition."
In addition to Abel, Florian and Vescey, the research was conducted byMichael M. Halassa of the Department of Psychiatry at Massachusetts General Hospitaland 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 ofMedicine. The research was supported by the National Institutes of Health.
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