Enlarge

Credit: USACAC.Army.Mil

Having a tough time recalling a phone number someone spoke a few minutes ago or forgetting items from a mental grocery list is not a sign of mental decline; in fact, it's natural.

Countless psychological experiments have shown that, on average, the longest sequence a normal person can recall on the fly contains about seven items. This limit, which psychologists dubbed the "magical number seven" when they discovered it in the 1950s, is the typical capacity of what's called the brain's working memory.

Now physicists have come up with a model of brain activity that seems to explain the reason behind the magical memory number.

If long-term memory is like a vast library of printed tomes, working memory is a chalkboard on which we rapidly scrawl and erase information. The chalkboard, which provides continuity from one thought to the next, is also a place for quick-and-dirty calculations. It turns the spoken words that make up a telephone number into digits that can be written down or used to reply logically to a question. Working memory is essential to carrying on conversations, navigating an unfamiliar city and copying the moves in a new workout video.

It's easy to test how much you can fit on this chalkboard. Just have a friend make a list of ten words or numbers. Read the list once, and then try to recall the items. Most people max out at seven or fewer.

It makes intuitive sense: as a mental list gets longer, people are more likely to make mistakes or forget items altogether. But why do the clusters of neurons in our brains produce such a small chalkboard?

In a paper published on Nov. 19 in the journal Physical Review Letters, Mikhail Rabinovich, a neuroscientist at the BioCircuits Institute at the University of California, San Diego and Christian Bick, a graduate student at the Max Planck Institute for Dynamics and Self-Organization in Göttingen, Germany, present a mathematical picture of how neurons fire when we recall a sequence of steps -- such as turn-by-turn driving directions, the digits of a phone number or the words in a sentence.

When we hear the phrase "It was the best of times, it was the worst of times," a cluster of neurons fires during each word. When one cluster fires, it suppresses the others momentarily, preventing the sentence from coming out scrambled.

In Rabinovich and Bick's model, the excitation of a certain cluster represents a single point. As the neurons for "It," "was," "the," and "best" fire in sequence, the brain creates pathways from one point, or brain state, to the next. The more powerfully each excited cluster can inhibit or suppress all others in the sequence from firing, the more solid these pathways.

When we recall the sentence, the brain follows these pathways from state to state to reproduce the sequence, like a tightrope walker hurrying along a wire from one perch to the next.

As a sentence or a string of numbers gets longer, it becomes exponentially harder for the excited cluster to suppress the others from firing, resulting in pathways that are weak or barely there. Recalling seven items requires about 15 times the suppression needed to recall three. Ten items requires inhibitory powers that are 50 times stronger, and 20 or more items would require suppression hundreds of times stronger still. That, Rabinovich explained, is normally not biologically feasible.

"Synapses can't be stronger than that," he said. "The brain is a very complex biochemical machine."

Mathematical models like these may seem removed from the gritty reality of gray matter and neural chemistry, according to Karl Friston, who directs the Wellcome Trust Centre for Neuroimaging at University College London, but they provide a critical connection between what people actually experience and the hidden mechanisms inside the brain.

Rabinovich's model, Friston said, "is both plausible and compelling." It correctly predicts the working memory's capacity and with a little elaboration could be tested experimentally. Friston said the model suggests patterns in the working memory's activity that should be discernible in the brain's electrical signals.

The exception to Rabinovich's model may be autistic individuals who skip effortlessly past seven and eight items, memorizing even a hundred random numbers in a single read-through. Their brains seem to be able to create much stronger pathways than the typical brain.

Source: Inside Science News Service

http://www.physorg.com/news178220995.html

Comment:
The problem with this article and the magic seven theory generally is that it only applies to language short term memory and only to unrelated sequential itemisation.  That is not a problem per se, but that claim that this is the limit of working memory is, because the actual limit is in the vicinity of 1,000 items, and it is fairly easy to demonstrate.

At any given moment you know where you are, what you are doing or intending to do, and what you planned to do next.  The number of items carried forward in working memory is quite vast.  These orientation cues can be lost and some brain lesions cause subjects to lose the ability to hold orientation cues.  They do not know where they are or what they are doing or what they intend to do - they are lost.

Apart from orientation cues, we hold information in numerous domains.  Consider a simple experiment.  A subject is led into a room, say a room in a house (that has the usual furniture, wall hangings etc) sat down and blind folded.  Now another experimenter enters the room and tests the short term store of the subject.  The subject will typically be able to remember around 500 items if the scope of items is explained before hand or up to 1,000 if primed.  Items include:
Various properties of the voice of the first experimenter, the words he/she used, the clothes they were wearing, some gestures, facial expressions, the path they walked, etc.  Around 125~250 items right there;
They will remember properties of the room they are in including its size, where the doors and windows are, colours, lamps, furniture, carpet, wall hanging and so on.  250~500 items;
They will remember why they are participating in the experiment, what they did up to the point when the second experimenter started the questions, what they have done since then, what they intend to do next, how they felt during the entire period and so on.  125~250 items.

We remember all this because it enters our working memory, that which we need for orientation in time and space.  Short term memory associated with language, serial unrelated items, however, comes it at around 5~7 items.

Try this.  Have a look at a photograph of a scene.  Then turn away, wait ten minutes, and then write down every single unique item that you remember about that scene in the photograph.  If you can't make a hundred then you really do have a poor memory.  Maybe after a month you'll be down to about seven items for that same photograph...

Posted by
Robert Karl Stonjek

Universitat Autňnoma de Barcelona (UAB, Spain) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps boost the production of the brain's stem cells -neurogenesis- and strengthens their differentiation in different types of neuron cells.

The research revealed that mice fed an LMN diet, when compared to those fed a control diet, have more cell proliferation in the two areas of the brain where neurogenesis is produced, the olfactory bulb and the hippocampus, both of which are greatly damaged in patients with Alzheimer's disease. These results give support to the hypothesis that a diet made up of foods rich in these antioxidant substances could delay the onset of this disease or even slow down its evolution.

The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology. Participating in the study were researchers from this department and from the departments of Cell Biology, Physiology and Immunology, and of Psychiatry and Legal Medicine, all of which are affiliated centres of the Institute of Neuroscience of Universitat Autňnoma de Barcelona. The company La Morella Nuts from Reus and the ACE Foundation of the Catalan Institute of Applied Neurosciences also collaborated in the study.

Polyphenols can be found in tea, beer, grapes, wine, olive oil, cocoa, nuts and other fruits and vegetables. Polyunsaturated fatty acids can be found in blue fish and vegetables such as corn, soya beans, sunflowers and pumpkins. The LMN cream used in this study was composed of a mixture of natural products: dried fruits and nuts, coconut, vegetable oils rich in polyunsaturated fat and flour rich in soluble fiber. These creams were created and patented by the company La Morella Nuts, located in Reus near Tarragona. Previous studies had verified their effects on regulating cholesterol levels and hypertension, two risk factors commonly associated with heart disease and Alzheimer's disease.

During the development of the brain, stem cells generate different neural cells (neurons, astrocytes and oligodendrocytes) which end up forming the adult brain. Until the 1960s it was thought that the amount of neurons in adult mammals decreased with age and that the body was not able to renew these cells. Now it is known that new neurons are formed in the adult brain. This generative capacity of the cells however is limited to two areas of the brain: the olfactory bulb and the hippocampus (area related to the memory and to cognitive processes). Although the rhythm of cell proliferation decreases with age and with neurodegenerative diseases, it is known that exercise and personal well being can combat this process.

The main objective of this research was to study the effect of an LMN cream-enriched diet on the neurogenesis of the brain of an adult mouse. Scientists used two groups of mice for the study. One group was given a normal diet and the other was given the same diet enriched with LMN cream. Both groups were fed during 40 days (approximately five years in humans). The analyses carried out in different brain regions demonstrated that those fed with LMN cream had a significantly higher amount of stem cells, as well as new differentiated cells, in the olfactory bulb and hippocampus.

The second objective was to verify if the LMN cream could prevent damage caused by oxidation or neural death in cell cultures. Cultures of the hippocampal and cortical cells were pretreated with LMN cream. After causing oxidative damage with hydrogen peroxide, which killed 40% of the cells, scientists observed that a pretreatment with LMN cream was capable of diminishing, and in some cases completely preventing, oxidative damage. The hippocampal and cortical cells were also damaged using amyloid beta (anomalous deposits of this protein are related to Alzheimer's disease). The results obtained were similar to those obtained using hydrogen peroxide.

These results demonstrate that an LMN diet is capable of inducing the generation of new cells in the adult brain, and of strengthening the neural networks which become affected with age and in neurogenerative processes such as Alzheimer's disease, as well as protecting neurons from oxidative and neural damage, two phenomena which occur at the origin of many diseases affecting the central nervous system.

In this study researchers have used different biochemical and molecular analysis techniques, with the help of specific antibodies, to detect different neuronal markers implied in the process of differentiation.

The group of researchers led by Dr Unzeta has spent years studying the effects oxidases have on oxidative stress as a factor implied in neurodegenerative disorders such as Parkinson and Alzheimer's disease, and the effects of different natural products with anti-inflammatory and antioxidant properties in different experimental models of Alzheimer's disease.

The study forms part of the CENIT project, which was awarded to La Morella Nuts in 2006 under the auspices of the INGENIO 2010 programme, with the objective of establishing methodologies for the design, evaluation and verification of functional foods which may protect against cardiovascular diseases and Alzheimer's disease. With 21.15m euros in funding and a duration of four years, the project has included the participation of 50 doctors and technicians from nine different companies, four universities (7 departments) and 2 research centres.

More information: "A diet enriched in polyphenols and polyunsaturated fatty acids, LMN diet, induces neurogenesis in the subventricular zone and hippocampus of adults mouse brain". Valente et al., 2009, Journal of Alzheimer's Disease, Volume 18:4. Valente T., Hidalgo, J., Bolea, I., Ramírez B., Anglés, N., Reguant, J., Morelló, J.R., Gutiérrez, C., Boada, M., Unzeta, M.

Source: Universitat Autonoma de Barcelona
http://www.physorg.com/news178279255.html

Posted by
Robert Karl Stonjek

A high-fat, high-sugar diet could have the same effect on brain chemistry as mood-altering drugs, giving scientific support to the craving for "comfort food", Australian researchers said Tuesday.

A controlled study of rats that were traumatised in early life and went on to exhibit depressed or anxious behaviours found those that were fed lard-laced foods such as cake or pie reversed their stress levels.

"We asked the question, if you're stressed early in life and then you're given yummy food to eat does that reduce your behavioural deficit, and basically that's what we found," lead researcher Margaret Morris told AFP.

"The animals who'd been exposed to stress who were then given palatable food, junk food if you will, no longer looked anxious."

Morris and her University of New South Wales team simulated trauma by forcing two control groups of rats to endure lengthy periods of separation from their mothers.

One of the groups was fed an all-you-can-eat "cafeteria diet" of junk food, and the other more healthy foods, and then run through a stress-testing maze.

Morris said they noticed an effect similar to anti-depressant drugs on the stressed rats after they ate junk food.

"The deficit in stress hormone receptors in part of the brain that we saw in the stressed animals was reversed by the diet," she said.

But Morris warned against hasty conclusions, saying more work needed to be done on the benefit of other factors such as exercise or the social interaction around food.

"We wouldn't want to say go and eat comfort food because that's not very healthy, but if we can find out whatever it was that started that process in train and find some other way of doing that, that would be really useful."

"There might be a critical time in the brain of those animals that their mood pathways or their behaviour is being modulated, and (if we) just tickled it for a few weeks maybe we would get the same benefit without having to make them all obese," she added.

(c) 2009 AFP
http://www.physorg.com/news178270511.html

Posted by
Robert Karl Stonjek

By playing the video game Rock Band for an hour, Kansas State University students were able to help a pair of psychology professors with their research to understand how people can achieve flow while at work or while performing skilled tasks.

Clive Fullagar, a professor, and Patrick Knight, an associate professor, found that -- like Goldilocks -- most people achieve flow with work that is neither too easy nor too hard but just right.

"For those students who have a moderate level of skill at Rock Band, the song has to be moderately challenging and match his or her skill level for optimal enjoyment to occur," Fullagar said. "That has broad implications for teaching. It means that if we want students to enjoy or get a lot of satisfaction out of classes, we need to assign them challenging tasks but make sure that they have the skills necessary to meet the challenges of those tasks."

In a psychology lab in K-State's Bluemont Hall, students played guitar in the game. In an adjacent room, the researchers watched a monitor with the same screen shot that the subjects saw. The researchers could control what songs students played and how much of the feedback they saw.

This isn't the first time that a video game has been used to study flow. Others have used Tetris, but Fullagar and Knight said that the nature of the game wouldn't have allowed them adequate control for this study. To make Tetris meet a player's ability level, researchers slowed down the rate at which the blocks fell onto the screen. This also limited performance because players couldn't finish as many lines.

"With Rock Band, it's the same speed and the same notes no matter what your ability level is," Knight said. "We can control that and look at differences in performance in a more objective way."

Flow is a state of mind that occurs when people become totally immersed in what they are doing and lose all sense of time. It's an intrinsically motivating state, which means that people are engaged in the task for the pure enjoyment of performing the task and not for some extrinsic reward.

In another study that tracked architecture students over the course of a semester, Fullagar found that achieving flow was likely to result in a good mood and have a positive impact on psychological health. The findings appeared in September in the Journal of Occupational and Organizational Psychology.

Research has shown that the types of work that lead people to achieve flow have some common traits, including being goal directed, providing feedback and giving a sense of meaning to the worker. Moreover, flow occurs only when the person feels in control of the process.

The researchers also have studied flow with architecture and music students but said that tasks that result in flow don't have to be creative or skill-intensive in an artistic sense. Knight said some graduate students describe achieving flow when analyzing their data. Fullagar had an accounting major in one of his classes describe achieving flow by filling out income tax returns.

"In speaking to her it made so much sense," Fullagar said. "She has this skill that can help somebody by having a meaningful impact on their financial situation. And every single income tax return presents a unique challenge. This shows that people find flow in very different areas."

In the future, Fullagar and Knight would like to study whether there's a group effect to flow.

"With Rock Band you can test several subjects at once as they play in a band," Fullagar said. "What happens when one member is in flow? Is there a contagion and do other people get in flow, or does it make them feel inferior?"

Knight said, "Another way we might look at that is what happens when one of the band members bombs out."

The researchers said other potential areas of study include the effect of having subjects help set their own goals and whether people in flow actually perform better or just perceive that they do.

Source: Kansas State University (news : web)
http://www.physorg.com/news178284517.html

Posted by
Robert Karl Stonjek

Feeding the clock: Cycles of feeding and fasting drive circadian gene expression in the liver

This is Christopher Vollmers in the lab at the Salk Institute. Credit: Top Image: Courtesy of the Salk Institute for Biological Studies Bottom Image: Courtesy of Christopher Vollmers

When you eat may be just as vital to your health as what you eat, found researchers at the Salk Institute for Biological Studies. Their experiments in mice revealed that the daily waxing and waning of thousands of genes in the liver -- the body's metabolic clearinghouse -- is mostly controlled by food intake and not by the body's circadian clock as conventional wisdom had it.

"If feeding time determines the activity of a large number of genes completely independent of the circadian clock, when you eat and fast each day will have a huge impact on your metabolism," says the study's leader Satchidananda (Satchin) Panda, Ph.D., an assistant professor in the Regulatory Biology Laboratory.

The Salk researchers' findings, which will be published in a forthcoming issue of the Proceedings of the National Academy of Sciences, could explain why shift workers are unusually prone to metabolic syndrome, diabetes, high cholesterol levels and obesity.

"We believe that it is not shift work per se that wreaks havoc with the body's metabolism but changing shifts and weekends, when workers switch back to a regular day-night cycle," says Panda.

In mammals, the circadian timing system is composed of a central circadian clock in the brain and subsidiary oscillators in most peripheral tissues. The master clock in the brain is set by light and determines the overall diurnal or nocturnal preference of an animal, including sleep-wake cycles and feeding behavior. The clocks in peripheral organs are largely insensitive to changes in the light regime. Instead, their phase and amplitude are affected by many factors including feeding time.

The clocks themselves keep time through the fall and rise of gene activity on a roughly 24-hour schedule that anticipates environmental changes and adapts many of the body's physiological function to the appropriate time of day.

"The liver oscillator in particular helps the organism to adapt to a daily pattern of food availability by temporally tuning the activity of thousands of genes regulating metabolism and physiology," says Panda. "This regulation is very important, since the absence of a robust circadian clock predisposes the organism to various metabolic dysfunctions and diseases."

Despite its importance, it wasn't clear whether the circadian rhythms in hepatic transcription were solely controlled by the liver clock in anticipation of food or responded to actual food intake.

To investigate how much influence rhythmic food intake exerts over the hepatic circadian oscillator, graduate student and first author Christopher Vollmers put normal and clock-deficient mice on strictly controlled feeding and fasting schedules while monitoring gene expression across the whole genome.

He found that putting mice on a strict 8-hour feeding/16-hour fasting schedule restored the circadian transcription pattern of most metabolic genes in the liver of mice without a circadian clock. Conversely, during prolonged fasting, only a small subset of genes continued to be transcribed in a circadian pattern even with a functional circadian clock present.

"Food-induced transcription functions like a metabolic sand timer that runs for 24 hours and is continually reset by the feeding schedule while the central circadian clock is driven by self-sustaining rhythms that help us anticipate food, based on our usual eating schedule," says Vollmers. "But in the real world we don't eat at the same time every day and it makes perfect sense to increase the activity of metabolic genes when you need them the most."

For example, genes that encode enzymes needed to break down sugars rise immediately after a meal, while the activity of genes encoding enzymes needed to break down fat is highest when we fast. Consequently a clearly defined daily feeding schedule puts the enzymes of metabolism in shift work and optimizes burning of sugar and fat.

"Our study represents a seminal shift in how we think about circadian cycles," says Panda. "The circadian clock is no longer the sole driver of rhythms in gene function, instead the phase and amplitude of rhythmic gene function in the liver is determined by feeding and fasting periods—the more defined they are, the more robust the oscillations become."

While the importance of robust metabolic rhythms for our health has been demonstrated by shift workers' increased risk of developing metabolic syndrome, the underlying molecular reasons are still unclear. Panda speculates that the oscillations serve one big purpose: to separate incompatible processes, such as the generation of DNA-damaging reactive oxygen species and DNA replication.

Panda, for one, has stopped eating between 8 pm and 8 am and says he feels great. "I even lost weight, although I eat whatever I want during the day," he says.

Source: Salk Institute (news : web)
http://www.physorg.com/news178369757.html

Posted by
Robert Karl Stonjek

(PhysOrg.com) -- You wouldn't want a car with no brakes. It turns out that the developing brain needs them, too.

Researchers at the Stanford University School of Medicine have identified a set of molecular brakes that stabilize the developing brain's circuitry. Moreover, experimentally removing those brakes in mice enhanced the animals' performance in a test of visual learning, suggesting a long-term path to therapeutic application.

In a study to be published Nov. 25 in Neuron, Carla Shatz, PhD, professor of neurobiology and of biology, and her colleagues have implicated two members of a large family of proteins critical to immune function (collectively known as HLA molecules in humans and MHC1 molecules in mice) in brain development. Until recently, these immune-associated molecules were thought to play no role at all in the healthy brain.

In previous studies, Shatz and her co-investigators have shown that MHC molecules are found on the surfaces of nerve cells in the brain, and that they temper "synaptic plasticity": the ease with which synapses — the more than 100 trillion points of contact between nerve cells that determine brain circuitry — are strengthened, weakened, created or destroyed in response to experience. In one recent study, the Shatz group tied two specific members of the MHC1 family, called K and D, to the ability of circuits in a brain region responsible for motor learning to be refined by a learning experience.

This time, the scientists looked at vision processing in the brain. "We'd already found that K and D were located in brain regions we knew mattered: the visual cortex, and a relay station in the brain that sends its input to the visual cortex," said Shatz.

A good example of the "use it or lose it" manner in which experience-dependent circuit tuning shapes the brain is the ability of one eye to take over brain circuits that normally would be used by the other eye.

"Normally, your two eyes share vision-devoted brain circuits 50/50," Shatz said. "But when kids are born with a congenital cataract, or lose an eye — or in animal models where one eye is blocked — so that the brain's visual-information-processing machinery is no longer being used evenly by both eyes, the other eye doesn't just sit there. It takes over the machinery normally reserved for input from the other eye."

In order to map the roles of K and D in visual development, Shatz's group studied mice genetically engineered to lack these two molecules. They found that developmental circuit tuning was abnormal, she said. "The nerve input from the eyes was the same at the gross level — the major nerve tracts still went from the eye to the first visual relay system, and from there to the visual cortex. But the detailed connections within each structure had been altered. The adult patterning didn't develop normally."

In these K- and D-deficient mice, the capacity of a more-used eye to dominate visual information-processing circuitry is abnormal, and in a surprising way, said Shatz. "There's too much of it," she said. "If one eye stops functioning, the other eye takes over more than its fair share of the cortical machinery devoted to the brain's visual-information-processing territory."

In a test of visual performance, Shatz's team showed that the K- and D-deficient mice could see better through their remaining eye than could ordinary mice raised with a similarly blocked eye. "This suggests there's some kind of molecular brake on plasticity in the brain, and these molecules are involved in the braking system. Taking off the brake improved performance," she said.

Using a new method for localizing molecules in three-dimensional chunks of tissue (pioneered by co-author Stephen Smith, PhD, professor of molecular and cellular physiology and a member of the Stanford Cancer Center), Shatz's team was able to show that K and D are located at synapses. "We've placed them at the scene of the crime, right where circuit change happens," she said. "We think that in the brain they're pieces of a common braking-system pathway."

What's going on in the brain that needs a brake in the first place? Without both accelerators and brakes, any dynamic system — such as the brain, where connections change dramatically in response to whether they're being used — would become unstable, Shatz said. "Some of us think epilepsy, for example, could be a consequence of this process being not carefully controlled and regulated, and happening too easily."

That MHC molecules are also expressed on neurons has very large implications, because inflammation works through the immune system. Inflammation triggers the release of molecules called cytokines that change MHC1 levels on cells throughout the body, said Shatz. "If this process also changes MCH1 levels on cells in the brain, could that alter the circuit-tuning process enough to make a difference in behavior?"

There are also therapeutic implications, Shatz observed. "Maybe in children with learning disabilities, the brake's been applied too hard — or it could mean that after injury to an adult's brain, taking the brake off or loosening it up a bit could allow the brain to get retrained more easily."

Source: Stanford University Medical Center (news : web)
http://www.physorg.com/news178374711.html

Posted by
Robert Karl Stonjek

Auditory illusion: How our brains can fill in the gaps to create continuous sound

It is relatively common for listeners to "hear" sounds that are not really there. In fact, it is the brain's ability to reconstruct fragmented sounds that allows us to successfully carry on a conversation in a noisy room. Now, a new study helps to explain what happens in the brain that allows us to perceive a physically interrupted sound as being continuous. The research, published by Cell Press in the November 25 issue of Neuron provides fascinating insight into the constructive nature of human hearing.

"In our day-to-day lives, sounds we wish to pay attention to may be distorted or masked by background noise, which means that some of the information gets lost. In spite of this, our brains manage to fill in the information gaps, giving us an overall 'image' of the sound," explains senior study author, Dr. Lars Riecke from the Department of Cognitive Neuroscience at Maastricht University in The Netherlands. Dr. Riecke and colleagues were interested in unraveling the neural mechanisms associated with this auditory continuity illusion, where a physically interrupted sound is heard as continuing through background noise.

The researchers investigated the timing of sensory-perceptual processes associated with the encoding of physically interrupted sounds and their auditory restoration, respectively, by combining behavioral measures where a participant rated the continuity of a tone, with simultaneous measures of electrical activity in the brain. Interestingly, slow brain waves called theta oscillations, which are involved in encoding boundaries of sounds, were suppressed during an interruption in a sound when that sound was illusorily restored. "It was as if a physically uninterrupted sound was encoded in the brain," says Dr. Riecke. This restoration-related suppression was most obvious in the right auditory cortex.

Taken together, the findings reveal a novel mechanism that enhances our understanding of the constructive nature of human hearing. "Our results revealed that spontaneous modulations in slow evoked auditory cortical oscillations may determine the perceived continuity of fragmented sounds in noise," concludes Dr. Riecke. Interestingly, the suppressive effect was present before an illusorily filled gap and reached maximum shortly after the gap's actual onset, suggesting that the mechanism may work rapidly or anticipatorily and thereby facilitate stable hearing of fragmented sounds in natural environments. The authors also suggest that their results might inspire future design of devices to assist people with hearing deficits.

Source: Cell Press (news : web)
http://www.physorg.com/news178376538.html

Posted by
Robert Karl Stonjek

An end to sleep problems? Researchers discover enzyme behind effects of sleep deprivation

There is hope for those who miss one night too many or whose children keep them up at night. The unwelcome effects of a bad night's sleep - forgetfulness, impaired mental performance - can be dealt with by reducing the concentration of an enzyme in the brain.

These are the conclusions of research published by Dutch researcher Robbert Havekes and colleagues in the 22 October issue of Nature.

Millions of people are regularly plagued by sleep deprivation. This can lead to both short-term and long-term problems with memory and learning capacity. How sleep deprivation causes these kinds of problems was largely unknown up to now. Havekes and his colleagues discovered that sleep deprivation in mice undermines the function of a specific molecular mechanism in the hippocampus, the area of the brain responsible for consolidating new memories.

Enzyme inhibition

The researchers kept mice awake for five hours. They found increased levels and activity of the enzyme PDE4 and lower levels of the molecule cAMP in these mice. cAMP plays a crucial role in the formation of new connections between brain cells in the hippocampus and the strengthening of old ones. And without these processes we cannot learn.

The researchers inhibited the activity of the PDE4 enzyme and discovered that this counteracts the effects of sleep deprivation. Lack of sleep leads to an increased PDE4 activity which then blocks the action of cAMP. Consequently fewer connections being formed or strengthened in the hippocampus. This is the first report of researchers 'saving' synaptic plasticity (the ability to develop and strengthen new connections) from the effects of sleep deprivation.

The discovery not only shows how a lack of sleep leads to problems, but also how these problems can be solved. Drugs that stimulate the action of cAMP may make it possible to counteract the effects of sleep deprivation.

Neurobiologist Robbert Havekes received a grant from NWO's Rubicon programme in 2007. Havekes is currently working with Ted Abel's group at the University of Pennsylvania.

More information: The article Sleep deprivation impairs cAMP signalling in the hippocampus by Christopher G. Vecsey, George S. Baillie, Devan Jaganath, Robbert Havekes, Andrew Daniels, Mathieu Wimmer, Ted Huang, Kim M. Brown, Xiang-Yao Li, Giannina Descalzi, Susan S. Kim, Tao Chen, Yu-Ze Shang, Min Zhuo, Miles D. Houslay & Ted Abel appeared in the 22 October issue of Nature.

Provided by Netherlands Organisation for Scientific Research
http://www.physorg.com/news178449806.html

Posted by
Robert Karl Stonjek