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[milosrajkovic]

by Sholim

[mummynotpig-blog]

[neurosciencestuff]

Study Explains Why Fainting Can Result From Blood Pressure Drug Used In Conjunction With Other Disorders

A new study led by a Canadian research team has identified the reason why prazosin, a drug commonly used to reduce high blood pressure, may cause lightheadedness and possible fainting upon standing in patients with normal blood pressure who take the drug for other reasons, such as the treatment of PTSD and anxiety.

According to University of British Columbia researcher and study team leader Dr. Nia Lewis, the body is in constant motion leading to changes in blood pressure with every activity. For example, when standing, the body copes with the sudden drop in blood pressure by constricting peripheral vessels to concentrate the blood in the areas that help stabilize the body.

This study found that prazosin prevents this process by blocking the α1-adrenoreceptor, a critical pathway that allows the vessels to constrict. This physiological response is dangerous for individuals with normal blood pressure who take prazosin to treat the symptoms of PTSD and anxiety, for the act of standing up can cause light-headedness and/or fainting.

The study, entitled “Initial orthostatic hypotension and cerebral blood flow regulation: effect of α1-adrenoreceptor activity,” is published in the American Journal of Physiology–Regulatory, Integrative and Comparative Physiology.

Methodology

Eight males and four females, with an average age of 25, and all of whom had normal blood pressure, were enrolled in the cross-over trial.  On day one of the study, participants were weighed, measured, and familiarized with the blood pressure monitoring equipment and procedures that would be used.

On the next visit, participants stayed overnight at the research facility in order to control for activity and diet. The following morning they were given either prazosin (1mg/20kg body weight) or a placebo, and instructed to lie down.  After 20 minutes, they were told to rise in one smooth motion from the lying-down position to standing, and their blood pressure and cerebral blood flow was continuously monitored. They were required to remain standing for three minutes or until they felt severe lightheadedness and dizziness, or felt as if they were about to faint.

On their third and final visit the participants underwent the same procedure as on the second visit. At this visit, however, they received the placebo if they had previously been given the medication, and vice versa.

Results

The investigators found that:

All but one of the 12 participants who took the medication experienced temporary dizziness or lightheadedness upon standing.

All participants who took the placebo were able to complete the three-minute standing test. By contrast, only 2 of the 12 were able to complete the standing test after taking prazosin.

After taking prazosin, none of the participants were able to attain normal blood pressure levels after standing. As a result, blood flow to the brain was reduced and subjects were unable to stand for 3 minutes as they began to experience the onset of fainting.

When the participants had taken prazosin, mean arterial blood pressure and systolic blood pressure was significantly lower—by 15 percent— when lying down compared to when they took the placebo. Mean arterial blood pressure also fell for a longer period (11 seconds versus eight for placebo) after participants stood up following consumption of the medication, resulting in a lower arterial pressure levels.

Blood flow to the brain, as measured by cerebral blood flow velocity, was not different when lying down. However, brain blood flow in the prazosin trial was reduced by 33 percent more than in than compared with the placebo trial.

Conclusions

“We were able to determine that, because prazosin shuts down a pathway that is critical to regulate blood pressure, the capacity to safely control blood flow to the brain was also reduced to a level that could induce fainting,” said Dr. Lewis. “No study has examined the effects of prazosin on the interaction between blood pressure and blood flow to the brain. The findings derived from this study show a mechanism of how prazosin causes fainting,” she explained.

Importance of the Findings

“This study highlights the importance of a key pathway in the body’s blood pressure system, known as the α1-adrenergic sympathetic pathway, in ensuring the recovery of blood pressure following standing and how important this pathway is in ensuring blood flow to the brain is not reduced to a level where fainting may occur,” said Dr. Lewis.

Additionally, this study provides a cautionary alert to those who are prescribed prazosin, for other conditions besides hypertension. 

[neurosciencestuff]

Neural “Synchrony” May be Key to Understanding How the Human Brain Perceives

Despite many remarkable discoveries in the field of neuroscience during the past several decades, researchers have not been able to fully crack the brain’s “neural code.” The neural code details how the brain’s roughly 100 billion neurons turn raw sensory inputs into information we can use to see, hear and feel things in our environment.

In a perspective article published in the journal Nature Neuroscience on Feb. 25, 2013, biomedical engineering professor Garrett Stanley detailed research progress toward “reading and writing the neural code.” This encompasses the ability to observe the spiking activity of neurons in response to outside stimuli and make clear predictions about what is being seen, heard, or felt, and the ability to artificially introduce activity within the brain that enables someone to see, hear, or feel something that is not experienced naturally through sensory organs.

Stanley also described challenges that remain to read and write the neural code and asserted that the specific timing of electrical pulses is crucial to interpreting the code. He wrote the article with support from the National Science Foundation (NSF) and the National Institutes of Health (NIH). Stanley has been developing approaches to better understand and control the neural code since 1997 and has published about 40 journal articles in this area.

“Neuroscientists have made great progress toward reading the neural code since the 1990s, but the recent development of improved tools for measuring and activating neuronal circuits has finally put us in a position to start writing the neural code and controlling neuronal circuits in a physiological and meaningful way,” said Stanley, a professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

With recent reports that the Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, progress toward breaking the neural code could begin to accelerate.

The potential rewards for cracking the neural code are immense. In addition to understanding how brains generate and manage information, neuroscientists may be able to control neurons in individuals with epilepsy and Parkinson’s disease or restore lost function following a brain injury. Researchers may also be able to supply artificial brain signals that provide tactile sensation to amputees wearing a prosthetic device.

Stanley’s paper highlighted a major challenge neuroscientists face: selecting a viable code for conveying information through neural pathways. A longstanding debate exists in the neuroscience community over whether the neural code is a “rate code,” where neurons simply spike faster than their background spiking rate when they are coding for something, or a “timing code,” where the pattern of the spikes matters. Stanley expanded the debate by suggesting the neural code is a “synchrony code,” where the synchronization of spiking across neurons is important.

A synchrony code argues the need for precise millisecond timing coordination across groups of neighboring neurons to truly control the circuit. When a neuron receives an incoming stimulus, an electric pulse travels the neuron’s length and triggers the cell to dump neurotransmitters that can spark a new impulse in a neighboring neuron. In this way, the signal gets passed around the brain and then the body, enabling individuals to see, touch, and hear things in the environment. Depending on the signals it receives, a neuron can spike with hundreds of these impulses every second.

“Eavesdropping on neurons in the brain is like listening to a bunch of people talk—a lot of the noise is just filler, but you still have to determine what the important messages are,” explained Stanley. “My perspective is that information is relevant only if it is going to propagate downstream, a process that requires the synchronization of neurons.”

Neuronal synchrony is naturally modulated by the brain. In a study published in Nature Neuroscience in 2010, Stanley reported finding that a change in the degree of synchronous firing of neurons in the thalamus altered the nature of information as it traveled through the pathway and enhanced the brain’s ability to discriminate between different sensations. The thalamus serves as a relay station between the outside world and the brain’s cortex.

Synchrony induced through artificial stimulation poses a real challenge for creating a wide range of neural representations. Recent technological advances have provided researchers with new methods of activating and silencing neurons via artificial means. Electrical microstimulation had been used for decades to activate neurons, but the technique activated a large volume of neurons at a time and could not be used to silence them or separately activate excitatory and inhibitory neurons. Stanley compared the technique with driving a car that has the gas and brake pedals welded together.

New research methods, such as optogenetics, enable activation and silencing of neurons in close proximity and provide control unavailable with electrical microstimulation. Through genetic expression or viral transfection, different cell types can be targeted to express specific proteins that can be activated with light.

“Moving forward, new technologies need to be used to stimulate neural activity in more realistic and natural scenarios and their effects on the synchronization of neurons need to be thoroughly examined,” said Stanley. “Further work also needs to be completed to determine whether synchrony is crucial in different contexts and across brain regions.”

[neurogra-blog]

Anna Maria Wieczorek o tym, jakie efekty przynoszą treningi mózgu i umysłu (pamięć, koncentracja, logiczne myślenie, szybkość), zwłaszcza u seniorów.

[neurosciencestuff]

Researchers discover workings of brain’s ‘GPS system’

Just as a global posi­tion­ing sys­tem (GPS) helps find your loca­tion, the brain has an inter­nal sys­tem for help­ing deter­mine the body’s loca­tion as it moves through its surroundings.

A new study from researchers at Prince­ton Uni­ver­sity pro­vides evi­dence for how the brain per­forms this feat. The study, pub­lished in the jour­nal Nature, indi­cates that cer­tain position-tracking neu­rons — called grid cells — ramp their activ­ity up and down by work­ing together in a col­lec­tive way to deter­mine loca­tion, rather than each cell act­ing on its own as was pro­posed by a com­pet­ing theory.

Grid cells are neu­rons that become elec­tri­cally active, or “fire,” as ani­mals travel in an envi­ron­ment. First dis­cov­ered in the mid-2000s, each cell fires when the body moves to spe­cific loca­tions, for exam­ple in a room. Amaz­ingly, these loca­tions are arranged in a hexag­o­nal pat­tern like spaces on a Chi­nese checker board.

“Together, the grid cells form a rep­re­sen­ta­tion of space,” said David Tank, Princeton’s Henry L. Hill­man Pro­fes­sor in Mol­e­c­u­lar Biol­ogy and leader of the study. “Our research focused on the mech­a­nisms at work in the neural sys­tem that forms these hexag­o­nal pat­terns,” he said. The first author on the paper was grad­u­ate stu­dent Cristina Dom­nisoru, who con­ducted the exper­i­ments together with post­doc­toral researcher Amina Kinkhabwala.

Dom­nisoru mea­sured the elec­tri­cal sig­nals inside indi­vid­ual grid cells in mouse brains while the ani­mals tra­versed a computer-generated vir­tual envi­ron­ment, devel­oped pre­vi­ously in the Tank lab. The ani­mals moved on a mouse-sized tread­mill while watch­ing a video screen in a set-up that is sim­i­lar to video-game vir­tual real­ity sys­tems used by humans.

She found that the cell’s elec­tri­cal activ­ity, mea­sured as the dif­fer­ence in volt­age between the inside and out­side of the cell, started low and then ramped up, grow­ing larger as the mouse reached each point on the hexag­o­nal grid and then falling off as the mouse moved away from that point.

This ramp­ing pat­tern cor­re­sponded with a pro­posed mech­a­nism of neural com­pu­ta­tion called an attrac­tor net­work. The brain is made up of vast num­bers of neu­rons con­nected together into net­works, and the attrac­tor net­work is a the­o­ret­i­cal model of how pat­terns of con­nected neu­rons can give rise to brain activ­ity by col­lec­tively work­ing together. The attrac­tor net­work the­ory was first pro­posed 30 years ago by John Hop­field, Princeton’s Howard A. Prior Pro­fes­sor in the Life Sci­ences, Emeritus.

The team found that their mea­sure­ments of grid cell activ­ity cor­re­sponded with the attrac­tor net­work model but not a com­pet­ing the­ory, the oscil­la­tory inter­fer­ence model. This com­pet­ing the­ory pro­posed that grid cells use rhyth­mic activ­ity pat­terns, or oscil­la­tions, which can be thought of as many fast clocks tick­ing in syn­chrony, to cal­cu­late where ani­mals are located. Although the Prince­ton  researchers detected rhyth­mic activ­ity inside most neu­rons, the activ­ity pat­terns did not appear to par­tic­i­pate in posi­tion calculations.

[neurosciencestuff]

To Make Mice Smarter, Add A Few Human Brain Cells

For more than a century, neurons have been the superstars of the brain. Their less glamorous partners, glial cells, can’t send electric signals, and so they’ve been mostly ignored.

Now scientists have injected some human glial cells into the brains of newborn mice. When the mice grew up, they were faster learners. The study, published Thursday in Cell Stem Cell, not only introduces a new tool to study the mechanisms of the human brain, it supports the hypothesis that glial cells — and not just neurons — play an important role in learning.

The scientific obsession with neurons really began at the end of the 19th century. Spanish anatomy professor Santiago Ramon y Cajal used a special dye to stain brain tissue. Under the microscope, neurons were revealed in exquisite detail. “A dense forest,” Ramón y Cajal called it — a field of little branching cells that would soon be named neurons.

With beautiful ink drawings, Ramón y Cajal painstakingly mapped neural networks and slowly developed the theory that neurons are the telegraph lines of thought (an idea later embraced by Schoolhouse Rock). Every idea and memory — every aspect of learning — could be traced back to the electric signals sent between neurons. Ramón y Cajal won the Nobel Prize for his work, and scientists focused on neurons for the next century.

But neurons aren’t the only cells in the brain.

“We’ve overlooked half the brain,” says Douglas Fields, a neuroscientist at the National Institutes of Health. “We’ve only been studying one kind of cell in the brain.” The other kind of cell — glial cells — are at least as abundant as neurons. But early scientists thought they were so boring they didn’t even merit a singular noun. “Glia is plural — there is no singular,” Fields says. “We have ‘neuron’ but we don’t have ‘glion.’ “

Glial cells lacked the ability to send electric signals, and most scientists thought they were housekeeping cells, helping provide nutrients and insulation.

It was only in the last decade or so that scientists realized glial cells were more than that. Special types of glial cells, called astrocytes, which are named for the star-like patterns of their cellular structure, have their own form of chemical signaling. They have the potential to coordinate whole groups of neurons. “Glia are in a position to regulate the flow of information through the brain,” Fields says. “This is all missing from our models.”

And there’s something else. This type of glial cell, these astrocytes, have changed a lot as humans have evolved, while neurons have pretty much stayed the same. A mouse neuron and a human neuron look so much alike, even experienced neuroscientists can’t tell them apart.

“I can’t tell the differences between a neuron from a bird or a mouse or a primate or a human,” says Steve Goldman, a neuroscientist at the University of Rochester who has studied brain cells for decades. But Goldman says glial cells are easy to tell apart.

“Human glial cells — human astrocytes — are much larger than those of lower species,” he says. “They have more fibers and they send those fibers out over greater distances.”

The thought is maybe these glial cells have played a role in making humans smarter. So Goldman teamed up with this wife, Maiken Nedergaard, to test this idea.

They injected some human glial cells into the brains of newborn mice. The mice grew up, and so did the human glial cells. The cells spread through the mouse brain, integrating perfectly with mouse neurons and, in some areas, outnumbering their mouse counterparts. All the while Goldman says the glial cells maintained their human characteristics.

“They very much thought that they were in the human brain, in terms of how they developed and integrated,” he says.

So what are these mice like, the ones with brains full of functioning human cells? Their neural circuitry is still just the same, so they act completely normal. They still socialize with other mice and still seem interested in mousey things.

But the researchers say these mice are measurably smarter. In classic maze tests, they learn faster. “They make many fewer errors, and it takes them less time to come to the appropriate answer,” Goldman says.

It might take a normal mouse four or five attempts to learn the correct route, for example. But a mouse with human brain cells could get it on the second try. Glial cells — those boring glial cells — somehow enhance learning.

In fact, they could be changing what it means to be a mouse, and that raises ethical questions for this kind of research.

“Maybe bioethicists have been a little bit too cavalier assuming that a mouse with some human brain cells in it is just your normal old mouse,” says Robert Streiffer, a bioethicist from the University of Wisconsin-Madison. “Well, it’s not going to be human, but that doesn’t mean it’s a normal old mouse either.”

Streiffer says it’s not just that these mice can get through a maze more quickly — they’re better at recognizing things that scare them. And perception of fear is one of the things bioethicists must weigh when they decide the types of experiments you can do on an animal.

“So you have to sort of step back and do some hardcore philosophy,” he says. Like, will these types of human-animal hybrids eventually get close enough to humanity that we would feel uncomfortable performing experiments on them?

The researchers in this study say we’re really, really far from that point. And if you want to investigate the role of glial cells, these hybrid mice are the best tools available.

[neurosciencestuff]

Is this peptide a key to happiness?

What makes us happy? Family? Money? Love? How about a peptide?

The neurochemical changes underlying human emotions and social behavior are largely unknown. Now though, for the first time in humans, scientists at UCLA have measured the release of a specific peptide, a neurotransmitter called hypocretin, that greatly increased when subjects were happy but decreased when they were sad.

The finding suggests that boosting hypocretin could elevate both mood and alertness in humans, thus laying the foundation for possible future treatments of psychiatric disorders like depression by targeting measureable abnormalities in brain chemistry.

In addition, the study measured for the first time the release of another peptide, this one called melanin concentrating hormone, or MCH. Researchers found that its release was minimal in waking but greatly increased during sleep, suggesting a key role for this peptide in making humans sleepy.

The study is published in the March 5 online edition of the journal Nature Communications.

“The current findings explain the sleepiness of narcolepsy, as well as the depression that frequently accompanies this disorder,” said senior author Jerome Siegel, a professor of psychiatry and director of the Center for Sleep Research at UCLA’s Semel Institute for Neuroscience and Human Behavior. “The findings also suggest that hypocretin deficiency may underlie depression from other causes.”

(Image: ALAMY)

[neurosciencestuff]

Some brain cells are better virus fighters

Viruses often spread through the brain in patchwork patterns, infecting some cells but missing others. New research at Washington University School of Medicine in St. Louis helps explain why. The scientists showed that natural immune defenses that resist viral infection are turned on in some brain cells but switched off in others.

“The cells that a pathogen infects can be a major determinant of the seriousness of brain infections,” says senior author Michael Diamond, MD, PhD, professor of medicine. “To understand the basis of disease, it is important to understand which brain regions are more susceptible and why.”

While some brain infections are caused by bacteria, fungi or parasites, often the cause is a virus, such as West Nile virus, herpesvirus or enteroviruses.

For their study, now available online in Nature Medicine, the researchers focused on granule cell neurons, a cell type that rarely becomes infected. They compared gene profiles in granule cells from the cerebellum with the activity in cortical neurons in the cerebral cortex, which are more vulnerable to infection.

The comparison revealed many differences, including a number of genes in cortical neurons that were less well-expressed—meaning that for those specific genes there were fewer copies of mRNA, the molecules that relay genetic information from DNA to the cell’s protein-making mechanisms.

Next, the researchers transferred individually 40 of those genes into cortical neurons and screened the cells for susceptibility to viral infection. The test highlighted three antiviral genes that are induced by interferon, an important immune system protein. When the expression level of these genes increased in cortical neurons, the cells’ susceptibility to viral infection decreased.

The researchers also identified mechanisms that make some of these changes in genetic programming happen: regulatory factors known as microRNA, and differences in the way DNA is modified in the cell nucleus, both of which can affect gene expression levels.

Some of the genetic changes are only helpful against specific viral families, while others are effective against a broader spectrum of viruses and bacteria. The scientists can’t say yet if the differences in infection susceptibility are driven by the need to prevent infection or if they are a byproduct of changes that help neurons in particular brain regions perform essential functions.

To learn more about how these innate immune genes help cells resist infection, Diamond and his colleagues are disabling them in the brains of mice.

[neurosciencestuff]

Deep Brain Stimulation shows promise for patients with chronic, treatment resistant Anorexia Nervosa

In a world first, a team of researchers at the Krembil Neuroscience Centre and the University Health Network have shown that Deep Brain Stimulation (DBS) in patients with chronic, severe and treatment-resistant Anorexia Nervosa (anorexia) helps some patients achieve and maintain improvements in body weight, mood, and anxiety.

The results of this trial, entitled Deep Brain Stimulation of the Subcallosal Cingulate Area for Treatment-Refractory Anorexia Nervosa: A Phase I Pilot Trial, are published in the medical journal The Lancet. The study is a collaboration between lead author Dr. Nir Lipsman a neurosurgery resident at the University of Toronto and PhD student at the Krembil Neuroscience Centre; Dr. Andres Lozano, a neurosurgeon, at the Krembil Neuroscience Centre of Toronto Western Hospital and a professor and chairman of neurosurgery at the University of Toronto, whose research lab was instrumental in conducting the DBS research; and Dr. Blake Woodside, medical director of Canada’s largest eating disorders program at Toronto General Hospital and a professor of psychiatry at the University of Toronto.

The phase one safety trial investigated the procedure in six patients who would likely continue with a chronic illness and/or die a premature death because of the severity of their condition. The study’s participants had an average age of 38, and a mean duration of illness of 18 years. In addition to the anorexia, all patients, except one, also suffered from psychiatric conditions such as major depressive disorder and obsessive-compulsive disorder. At the time of the study, all patients currently, or had previously, suffered multiple medical complications related to their anorexia – altogether, the six patients had a history of close to 50 hospitalizations during their illnesses.

Study participants were treated with Deep Brain Stimulation (DBS), a neurosurgical procedure that moderates the activity of dysfunctional brain circuits. Neuroimaging has shown that there are both structural and functional differences between anorexia patients and healthy controls in brain circuits which regulate mood, anxiety, reward and body-perception.

Patients were awake when they underwent the procedure which implanted electrodes into a specific part of the brain involved with emotion, and found to be highly important in disorders such as depression. During the procedure, each electrode contact was stimulated to look for patient response of changes in mood, anxiety or adverse effects. Once implanted, the electrodes were connected to an implanted pulse generator below the right clavicle, much like a heart pacemaker.

Testing of patients was repeated at one, three, and six-month intervals after activation of the pulse generator device. After a nine-month period following surgery, the team observed that three of the six patients had achieved weight gain which was defined as a body-mass index (BMI) significantly greater than ever experienced by the patients. For these patients, this was the longest period of sustained weight gain since the onset of their illness. Furthermore, four of the six patients also experienced simultaneous changes in mood, anxiety, control over emotional responses, urges to binge and purge and other symptoms related to anorexia, such as obsessions and compulsions. As a result of these changes, two of these patients completed an inpatient eating disorders program for the first time in the course of their illness.

“We are truly ushering in a new of era of understanding of the brain and the role it can play in certain neurological disorders,” says Dr. Lozano. “By pinpointing and correcting the precise circuits in the brain associated with the symptoms of some of these conditions, we are finding additional options to treat these illnesses.”

While the treatment is still considered experimental, it is believed to work by stimulating a specific area of the brain to reverse abnormalities linked to mood, anxiety, emotional control, obsessions and compulsions all of which are common in anorexia. In some cases after surgery, patients are then able to complete previously unsuccessful treatments for the disease. The research may not only provide an additional therapy option for these patients in the future, but also furthers practitioners’ understanding of anorexia and the factors that cause it to be persistent.

“There is an urgent need for additional therapies to help those suffering from severe anorexia,” says Dr. Woodside. “Eating disorders have the highest death rate of any mental illness and more and more women are dying from anorexia. Any treatment that could potentially change the natural course of this illness is not just offering hope but saving the lives for those that suffer from the extreme form of this condition.”

A leading international expert in the field of DBS research, Dr. Lozano has been exploring the potential of DBS to treat a variety of conditions. Most recently, his team began the first ever DBS trial of patients with early Alzheimer’s disease, and showed that stimulation may help improve memory. This trial has now entered its second phase and expanded to medical centres in the United States.

[neurosciencestuff]

Solving the ‘Cocktail Party Problem’

Many smartphones claim to filter out background noise, but they’ve got nothing on the human brain. We can tune in to just one speaker at a noisy cocktail party with little difficulty—an ability that has been a scientific mystery since the early 1950s. Now, researchers argue that the competing noise of other partygoers is filtered out in the brain before it reaches regions involved in higher cognitive functions, such as language and attention control. Their experiments were the first to demonstrate this process.

The scientists didn’t do anything as social as attend a noisy party. Instead, Charles Schroeder, a psychiatrist at the Columbia University College of Physicians and Surgeons in New York City, and colleagues recorded the brain activity of six people with intractable epilepsy who required brain surgery. In order to identify the part of their brains responsible for seizures, the patients underwent 1 to 4 weeks of observation through electrocorticography (ECoG), a technique that provides precise neural recordings via electrodes placed directly on the surface of the brain. Schroeder and his team, using the ECoG data, conducted their experiments during this time.

The researchers showed the patients two videos simultaneously, each of a person telling a 9- to 12-second story; they were asked to concentrate on just one speaker. To determine which neural recordings corresponded to the “ignored” and “attended” speech, the team reconstructed speech patterns from the brain’s electrical activity using a mathematical model. The scientists then matched the reconstructed patterns with the original patterns coming from the ignored and attended speakers.

The patients’ brains had registered both attended and ignored speech, though they showed some preference for the attended speech, the researchers report online in Neuron. Because the researchers were able to record several regions of the patients’ brains, they saw that regions associated with “higher-order” abilities—like the inferior frontal cortex, which is involved with language—had only representations of attended speech. Moreover, this representation of attended speech improved as the speaker’s story unfolded. These findings support a continuous model of attention—called the “selective entrainment hypothesis”—in which the brain tracks and becomes increasingly selective to a particular voice.

The research supports the selective entrainment hypothesis, agrees Jason Bohland, director of Boston University’s Quantitative Neuroscience Laboratory, but it “doesn’t necessarily tell us how that happens. That’s a really hard question, and is still left very much up in the air.”

Though a technology less-invasive than ECoG would be needed, Bohland and Schroeder agree that this research could help provide good clinical markers for people with certain social disorders. People with attention deficit disorder, for example, may struggle in tracking specific voices or filtering out unwanted neural representations of sounds. And those problems should be represented in their brain activity.

Schroeder explained that this study was a part of a new wave of research that aims to “approximate a map of the total brain circuit that’s involved in [complex] things like speech and music perception, which people consider—rightly or wrongly—to be uniquely human.”

[neurosciencestuff]

One region, two functions: Brain cells’ multitasking may be a key to understanding overall brain function

A region of the brain known to play a key role in visual and spatial processing has a parallel function: sorting visual information into categories, according to a new study by researchers at the University of Chicago.

Primates are known to have a remarkable ability to place visual stimuli into familiar and meaningful categories, such as fruit or vegetables. They can also direct their spatial attention to different locations in a scene and make spatially-targeted movements, such as reaching.

The study, published in the March issue of Neuron, shows that these very different types of information can be simultaneously encoded within the posterior parietal cortex. The research brings scientists a step closer to understanding how the brain interprets visual stimuli and solves complex tasks.

“We found that multiple functions can be mapped onto a particular region of the brain and even onto individual brain cells in that region,” said study author David Freedman, PhD, assistant professor of neurobiology at the University of Chicago. “These functions overlap. This particular brain area, even its individual neurons, can independently encode both spatial and cognitive signals.”

Freedman studies the effects of learning on the brain and how information is stored in short-term memory, with a focus on the areas that process visual stimuli. To examine this phenomenon, he has taught monkeys to play a simple video game in which they learn to assign moving visual patterns into categories.

“The task is a bit like a baseball umpire calling balls and strikes,” he said, “since the monkeys have to sort the various motion patterns into two groups, or categories.”

The monkeys master the tasks over a few weeks of training. Once they do, the researchers record electrical signals from parietal lobe neurons while the subjects perform the categorization task. By measuring electrical activity patterns of these neurons, the researchers can decode the information conveyed by the neurons’ activity.

“The activity patterns in these parietal neurons carry strong information about the category that each motion pattern gets assigned to during the task,” Freedman said.

(Image: Thinkstock)

[neurosciencestuff]

World premiere of muscle and nerve controlled arm prosthesis

For the first time an operation has been conducted, at Sahlgrenska University Hospital, where electrodes have been permanently implanted in nerves and muscles of an amputee to directly control an arm prosthesis. The result allows natural control of an advanced robotic prosthesis, similarly to the motions of a natural limb.

A surgical team led by Dr Rickard Brånemark, Sahlgrenska University Hospital, has carried out the first operation of its kind, where neuromuscular electrodes have been permanently implanted in an amputee. The operation was possible thanks to new advanced technology developed by Max Ortiz Catalan, supervised by Rickard Brånemark at Sahlgrenska University Hospital and Bo Håkansson at Chalmers University of Technology.

“The new technology is a major breakthrough that has many advantages over current technology, which provides very limited functionality to patients with missing limbs,” says Rickard Brånemark.

Big challenges There have been two major issues on the advancement of robotic prostheses: 1) how to firmly attach an artificial limb to the human body; 2) how to intuitively and efficiently control the prosthesis in order to be truly useful and regain lost functionality.

“This technology solves both these problems by combining a bone anchored prosthesis with implanted electrodes,” said Rickard Brånemark, who along with his team has developed a pioneering implant system called Opra, Osseointegrated Prostheses for the Rehabilitation of Amputees.

A titanium screw, so-called osseointegrated implant, is used to anchor the prosthesis directly to the stump, which provides many advantages over a traditionally used socket prosthesis.

“It allows complete degree of motion for the patient, fewer skin related problems and a more natural feeling that the prosthesis is part of the body. Overall, it brings better quality of life to people who are amputees,” says Rickard Brånemark.

How it works Presently, robotic prostheses rely on electrodes over the skin to pick up the muscles electrical activity to drive few actions by the prosthesis. The problem with this approach is that normally only two functions are regained out of the tens of different movements an able-body is capable of. By using implanted electrodes, more signals can be retrieved, and therefore control of more movements is possible. Furthermore, it is also possible to provide the patient with natural perception, or “feeling”, through neural stimulation.

“We believe that implanted electrodes, together with a long-term stable human-machine interface provided by the osseointegrated implant, is a breakthrough that will pave the way for a new era in limb replacement,” says Rickard Brånemark.

The patient The first patient has recently been treated with this technology, and the first tests gave excellent results. The patient, a previous user of a robotic hand, reported major difficulties in operating that device in cold and hot environments and interference from shoulder muscles. These issues have now disappeared, thanks to the new system, and the patient has now reported that almost no effort is required to generate control signals. Moreover, tests have shown that more movements may be performed in a coordinated way, and that several movements can be performed simultaneously.

“The next step will be to test electrical stimulation of nerves to see if the patient can sense environmental stimuli, that is, get an artificial sensation. The ultimate goal is to make a more natural way to replace a lost limb, to improve the quality of life for people with amputations,” says Rickard Brånemark.

[neurosciencestuff]

Has evolution given humans unique brain structures?

Humans have at least two functional networks in their cerebral cortex not found in rhesus monkeys. This means that new brain networks were likely added in the course of evolution from primate ancestor to human. These findings, based on an analysis of functional brain scans, were published in a study by neurophysiologist Wim Vanduffel (KU Leuven and Harvard Medical School) in collaboration with a team of Italian and American researchers.

Our ancestors evolutionarily split from those of rhesus monkeys about 25 million years ago. Since then, brain areas have been added, have disappeared or have changed in function. This raises the question, ‘Has evolution given humans unique brain structures?’. Scientists have entertained the idea before but conclusive evidence was lacking. By combining different research methods, we now have a first piece of evidence that could prove that humans have unique cortical brain networks.

Professor Vanduffel explains: “We did functional brain scans in humans and rhesus monkeys at rest and while watching a movie to compare both the place and the function of cortical brain networks. Even at rest, the brain is very active. Different brain areas that are active simultaneously during rest form so-called ‘resting state’ networks. For the most part, these resting state networks in humans and monkeys are surprisingly similar, but we found two networks unique to humans and one unique network in the monkey.”

“When watching a movie, the cortex processes an enormous amount of visual and auditory information. The human-specific resting state networks react to this stimulation in a totally different way than any part of the monkey brain. This means that they also have a different function than any of the resting state networks found in the monkey. In other words, brain structures that are unique in humans are anatomically absent in the monkey and there no other brain structures in the monkey that have an analogous function. Our unique brain areas are primarily located high at the back and at the front of the cortex and are probably related to specific human cognitive abilities, such as human-specific intelligence.”

The study used fMRI (functional Magnetic Resonance Imaging) scans to visualise brain activity. fMRI scans map functional activity in the brain by detecting changes in blood flow. The oxygen content and the amount of blood in a given brain area vary according to a particular task, thus allowing activity to be tracked.

[neurosciencestuff]

Modeling Alzheimer’s disease using iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness

Working with a group from Nagasaki University, a research group at the Center for iPS Cell Research and Application (CiRA) has successfully modeled Alzheimer’s disease (AD) using both familial and sporadic patient-derived induced pluripotent stem cells (iPSCs), and revealed stress phenotypes and differential drug responsiveness associated with intracellular amyloid β oligomers in AD neurons and astrocytes.

In a study published online in Cell Stem Cell, Associate Professor Haruhisa Inoue and his team at CiRA and a research group led by Professor Nobuhisa Iwata of Nagasaki University generated cortical neurons and astrocytes from iPSCs derived from two familial AD patients with mutations in amyloid precursor protein (APP), and two sporadic AD patients. The neural cells from one of the familial and one of the sporadic patients showed endoplasmic reticulum (ER)-stress and oxidative-stress phenotypes associated with intracellular Aβ oligomers. The team also found that these stress phenotypes were attenuated with docosahexaenoic acid (DHA) treatment. These findings may help explain the variable clinical results obtained using DHA treatment, and suggest that DHA may in fact be effective only for a subset of patients. Using both familial and sporadic AD iPSCs, the researchers discovered that pathogenesis differed between individual AD patients. For example, secreted Aβ42 levels were depressed in familial AD with APP E693Δ mutation, elevated in familial AD with APP V717L mutation, but normal in sporadic AD.

“This shows that patient classification by iPSC technology may contribute to a preemptive therapeutic approach toward AD,” said Inoue, a principal investigator at CiRA who is also a research director for the CREST research program funded by the Japan Science and Technology Agency. “Further advances in iPSC technology will be required before large-scale analysis of AD patient-specific iPSCs is possible.”

[neurosciencestuff]

Small groups of brain cells store concepts for memory formation– from Luke Skywalker to your grandmother

Concepts in our minds – from Luke Skywalker to our grandmother - are represented by their own distinct group of neurons, according to new research involving a University of Leicester neuroscientist.

The research, by neuroscientist Professor Rodrigo Quian Quiroga from the University of Leicester Centre for Systems Neuroscience together with Professor Itzhak Fried, of the UCLA David Geffen School of Medicine, Tel Aviv Sourasky Medical Center and Tel Aviv University, and Professor Christof Koch, of the California Institute of Technology and Allen Institute for Brain Science, Seattle, is featured in a recent article of the prestigious Scientific American magazine.

Recent experiments during brain surgeries have shown that small groups of brain cells are responsible for encoding memories of specific people or objects.

These neurons may also represent different variations of one thing – from the name of a person to their appearance from many different viewpoints.

The researchers believe that single concepts may be held in as little as thousands of neurons or less – a tiny fraction of the billion or so neurons contained in the medial temporal lobe, which is a memory related structure within the brain.

The group were able to monitor the brain activity of consenting patients undergoing surgery to treat epilepsy. This allowed the team to monitor the activity of single neurons in conscious patients while they looked at images on laptop screens, creating and recalling memories.

In previous experiments, they had found that single neurons would ‘fire’ for specific concepts – such as Luke Skywalker – even when they were viewing images of him from different angles or simply hearing or reading his name.

They have also found that single neurons can also fire to related people and objects – for instance, the neuron that responded to Luke Skywalker also fired to Yoda, another Jedi from Star Wars.

They argue that relatively small groups of neurons hold concepts like Luke Skywalker and that related concepts such as Yoda are held by some but not all of the same neurons. At the same time, a completely separate set of neurons would hold an unrelated concept like Jennifer Aniston.

The group believes this partially overlapping representation of related concepts are the neural underpinnings of encoding associations, a key memory function.

Professor Quian Quiroga said: “After the first thrill when finding neurons in the human hippocampus with such remarkable firing characteristics, converging evidence from experiments we have been carrying out in the last years suggests that we may be hitting one of the key mechanisms of memory formation and recall.

“The abstract representation of concepts provided by these neurons is indeed ideal for representing the meaning of the sensory stimuli around us, the internal representation we use to form and retrieve memories. These concepts cells, we believe, are the building blocks of memory functions.”

[neurogra-blog]

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