Posts tagged science
Articles and news from the latest research reports.
Figure 1: Typical slow gamma (left), fast gamma (center) and theta (right) brain-wave patterns measured during voluntary actions in rats.
Banding together to control movement
Synchrony is critical for the proper functioning of the brain. Synchronous firing of neurons within regions of the brain and synchrony between brain waves in different regions facilitate information processing, yet researchers know very little about these neural codes. Now, new research led by Tomoki Fukai of the RIKEN Brain Science Institute reveals how one region of the brain uses multiple brain-wave frequency bands to control movement.
Control of movement requires activation of numerous muscle groups in correct sequence, a function achieved by the motor cortex. To investigate the contribution of brain waves to this process, Fukai and his colleagues inserted multi-channel electrodes into the motor cortex of rats to record brain-wave patterns as the animals learned to push, hold and then pull a lever to obtain a food reward. They also developed a machine-learning technique to extract spike sequences of individual neurons from the recorded waves.
Fukai and his colleagues found that brain waves of different frequencies appeared during distinct stages of the movements. Fast gamma waves, with frequencies of around 100 hertz, were most prominent when the rats pushed or pulled the lever, whereas slow gamma waves, with frequencies of 25–40 hertz, peaked when the rats held the lever to prepare for the next pull. Theta waves (4–10 hertz) peaked while the rats held the lever, and the initiation of the pulling movement coincided with a specific phase of these oscillations (Fig. 1).
Both frequencies of gamma waves were coupled to the theta waves such that the peaks of all three brain-wave frequencies occurred at the same time. The activity of different types of nerve cells in different layers of the motor cortex was also synchronized with specific brain-wave frequencies. Importantly, cells encoding different stages of the sequential movements fired in distinct phases of the theta waves.
The results suggest that theta waves play an important role in coordinating the neuronal activity underlying the planning and execution of voluntary movement. Theta waves are known to be important for the processing of spatial information in the hippocampus, but this is the first time that a similar code has been observed in the motor cortex.
“We are currently using machine-learning techniques to study how phase-locked spikes in different layers of the motor cortex encode motor information,” says Fukai. “We are also studying whether a similar oscillatory coordination takes place in the prefrontal cortex during decision-making.”
Mechanism behind the activation of dormant memory cells discovered
The electrical stimulation of the hippocampus in in-vivo experiments activates precisely the same receptor complexes as learning or memory recall. This has been discovered for the first time and the finding has now been published in the highly respected journal “Brain Structure Function”. “This may form the basis for the use of medications aimed at powering up dormant or less active memory cells,” says Gert Lubec, Head of Fundamental Research / Neuroproteomics at the University Department of Paediatrics and Adolescent Medicine at the MedUni Vienna.
“This discovery has far-reaching consequences both for the molecular understanding of memory formation and the understanding of the clinical electrical stimulation, which is already possible, of areas of the brain for therapeutic purposes,” says the MedUni Vienna researcher. Similar principles are currently already being used in the field of deep brain stimulation. With this technology, an implanted device delivers electronic impulses to the patient’s brain. This physical stimulation allows neuronal circuits to be influenced that control both behaviour and memory.
The latest findings very much form part of the highly controversial subject of “cognitive enhancement”. Scientists are currently discussing the possibility of improving mental capacity through the use of drugs - including in healthy subjects of all age groups, but especially in patients with age-related impairments of cognitive processes.
With regard to the study design, two electrodes were implanted into the brain in an animal model. One transferred electrical impulses to stimulate the hippocampus, while the other transferred the electrical signals away. “These electrical potentials are the electrical equivalent of memory and are known as LTP (Long Term Potentiation),” explains Lubec. The generation of LTP in an in-vivo experiment was accompanied by specific changes in the receptor complexes - the same receptor complexes that are also activated during learning and memory formation.
Geneticists Show How Molecular Switches Coordinate the Nervous System
Geneticists from Trinity College Dublin interested in ‘reverse engineering’ the nervous system have made an important discovery with wider implications for repairing missing or broken links. They found that the same molecular switches that induce originally non-descript cells to specialise into the billions of unique nerve cell types are also responsible for making these nerve cells respond differently to the environment.
The geneticists are beginning to understand how these molecular switches, called ‘transcription factors’, turn on specific cellular labels to form complex bundles of nerves. These bundles function to ensure we respond and react appropriately to the incredible amount of information our brains encounter. Understanding how to precisely program nerve cells could help to target missing or broken links following serious injury or the onset of degenerative diseases such as Alzheimer’s or Parkinson’s.
Commenting on the importance and wider implications of this discovery, Assistant Professor in Genetics at Trinity, Juan Pablo Labrador said: “We know very little of how individual nerve cells are programmed to assemble into specific nerves in living organisms to make specific circuits, so our work is like reverse engineering the nervous system.”
“To restore damaged or missing connections in the nervous system – for example, after spinal cord injuries or degenerative diseases such as Alzheimer’s or Parkinson’s – we need to know how nerve cells are programmed to make those connections in the first place. For that we require a complex ‘builder’s manual’ that tells us how to program the neurons to make the connections. What we are doing in my lab is trying to write this manual.”
The nervous system can be thought of as an incredibly complex network of wires, which are all arranged into different, related bundles to coordinate complex tasks. The wires are the cellular extensions from the individual nerve cells that assemble into bundles to form specific nerves. The geneticists have begun to understand how varied combinations of transcription factors work to generate different nerve cells and direct their wiring to form specific nerves.
By studying the behaviour of individual nerve cells that make connections with muscles, the geneticists discovered specific ‘footprints’ of labels that induced these nerve cells to assemble into specific bundles that link to their target muscles. Individual transcription factors are only able to turn on specific labels to some extent. It is only the action of all of them together that programmes the nerve cells to turn on all the labels required.
The research was just published in the high-profile journal Neuron. The team led by Assistant Professor Juan Pablo Labrador, found that the actions of the transcription factor influencing nerve cell differentiation in flies (‘Eve’) controls nerve cell surface labels.
The team also showed that if these labels, targeted by Eve, are expressed erroneously, the nerve cells will not form the correct nerves. Additionally, the team discovered that different combinations of transcription factors including Eve work as codes for different groups of labels that guide individual nerve development.
(Source: tcd.ie)
Seizing Control of Brain Seizures
A few years after serving in the Israeli army during the first Gulf War, Daniela Kaufer made a startling discovery about the effect of psychological stress on the brain. As a graduate student at the Hebrew University she showed that the kind of extreme stress experienced in combat can break down the physiological barriers that normally protect the brain.
She could not have known it then, but the finding would eventually lead her to uncover a key change in brain chemistry that triggers epileptic seizures. The Bakar Fellows Program is now helping her refine a strategy to block the threat and protect the brain from damage caused by physical trauma and other insults.
A physiological line of defense normally prevents circulating blood from entering the brain. Known as the blood-brain barrier, the tightly controlled system buffers the brain from exposure to bacteria and other blood-borne invaders. Kaufer’s research has revealed how brain trauma can disrupt brain function once the barrier is breached.
In lab research as a postdoc at Stanford in 2002, Kaufer and her Israeli colleague Alon Friedman examined what happens in the brain when the barrier is compromised. They found that seizures were likely if – and only if – the brain came in contact with blood that had been circulating in the body.
They showed that a very common protein in blood called albumin accelerates signaling between neurons to abnormal levels. Neurons become overexcited and can cause seizures.
“We were surprised, even a little disappointed, that it was such a common component of the blood – nothing exotic at all – that led to epilepsy,” recalls Kaufer, associate professor of integrative biology.
She and Friedman went to on to show that albumin interacts with a ubiquitous cell protein called TGF-Beta receptor to cause the damage.
In the healthy brain, TGF-Beta signaling affects activity of star-shaped sister cells of neurons called astrocytes, which normally limit neuron-to-neuron firing signals across the synapse. But when albumin stimulates TGF-Beta receptors, astrocytes lose some of their control. Neuron signaling spikes dangerously, and promotes the development of epileptic seizures.
“Researchers knew that following traumatic brain injury the risk of epilepsy was great, but they didn’t know why,” Kaufer says.
As luck would have it, a prescription drug for hypertension blocks TGF-Beta signaling. With support from the Bakar Fellows program, Kaufer is now carrying out research to confirm that blocking abnormal TGF-Beta activity can prevent epilepsy from a range of insults.
She expects that her and Friedman’s lab research, coupled with clinical studies, will demonstrate the drug’s ability to protect the brain and move it into use in emergency medicine to prevent victims of brain trauma from becoming epileptic.
Kaufer and Friedman’s research is suggesting too that a number of assaults besides physical trauma – from brain infections to stroke – can also weaken the blood-brain barrier, and lead to the development of epilepsy through TGF-beta signaling. Emergency medicine physicians need only determine if the barrier has been breached to know if a patient is at risk for seizures.
Fortunately, the condition of the blood-brain barrier can be assessed using a safe and straightforward FDA-approved MRI protocol, so screening for epilepsy risk is within reach, says Kaufer.
“Right now, if someone comes to the emergency room with traumatic brain injury, they have a 10 to 50 percent chance of developing epilepsy. But you don’t know which ones, nor do you have a way of preventing it. And epilepsy from brain injuries is the type most unresponsive to drugs.
“I’m very hopeful and that our research can spare these patients the added trauma of epilepsy.”
Surprising culprit found in cell recycling defect
To remain healthy, the body’s cells must properly manage their waste recycling centers. Problems with these compartments, known as lysosomes, lead to a number of debilitating and sometimes lethal conditions.
Reporting in the Proceedings of the National Academy of Sciences (PNAS), researchers at Washington University School of Medicine in St. Louis have identified an unusual cause of the lysosomal storage disorder called mucolipidosis III, at least in a subset of patients. This rare disorder causes skeletal and heart abnormalities and can result in a shortened lifespan. But unlike most genetic diseases that involve dysfunctional or missing proteins, the culprit is a normal protein that ends up in the wrong place.
Image caption: In normal cells, phosphotransferase (green) is shown overlapping with the Golgi apparatus (red), which indicates that phosphotransferase is located in the Golgi, where it should be (Credit: Eline van Meel, PhD)
“There is a lot of interest and study about how cells distribute proteins to the right parts of the cell,” said senior author Stuart A. Kornfeld, MD, PhD, the David C. and Betty Farrell Professor of Medicine. “Our study has identified one of the few examples of a genetic disease caused by the misplacement of a protein. The protein functions just fine. It just doesn’t stay in the right place.”
The right place, in this case, is the Golgi apparatus, the cell’s protein packaging center. The protein in question – phosphotransferase – normally resides in the Golgi, where its job is to attach address labels to proteins bound for the lysosome. There are 60 such lysosomal proteins, and all of them must be properly labeled if they are to end up in a lysosome, where they recycle waste.
Image caption: In mutant cells, the protein phosphotransferase (green) is spread beyond the Golgi (red). Outside the Golgi, this wayward phosphotransferase is no longer able to perform its job of properly addressing enzymes bound for the lysosome (Credit: Eline van Meel, PhD)
Kornfeld and his colleagues, including first author Eline van Meel, PhD, postdoctoral research associate, showed that the phosphotransferase protein responsible for adding the address label starts out in the Golgi as it should, but seems to lack the signal to keep it there.
“Under normal circumstances, the phosphotransferase moves up through the Golgi, but then it’s recaptured and sent back,” Kornfeld said. “Our study shows that the mutant phosphotransferase moves up but is not recaptured. Ironically, the phosphotransferase that escapes the Golgi ends up in the lysosomes, where it is degraded.”
Because phosphotransferase gradually wanders away from the Golgi, a low level of lysosomal enzymes end up being properly addressed, but at perhaps 20 percent of the normal amount.
“In many lysosomal storage disorders, such as Tay-Sachs or Gaucher’s disease, only one out of the 60 enzymes is missing from the lysosome,” Kornfeld said. “But the mislocalization of phosphotranferase causes the misdirection of all 60 lysosomal enzymes.”
While the errant phosphotransferase ends up being degraded in the lysosome, the resulting misdirected lysosomal proteins end up in the bloodstream. As a result, children with this disorder have lysosomal proteins in their blood at levels 10 to 20 times higher than normal. But because some get to the lysosome at a low level, people with mucolipidosis III don’t have the most severe form of the disease.
“Type III patients live into adulthood, but they’re very impaired,” said Kornfeld. “They have joint and heart problems and have trouble walking. In the most severe form, type II, there is zero activity of phosphotransferase. None of the 60 enzymes are properly tagged, so these patients’ lysosomes are empty. Children with type II usually die by age 10.”
Having implicated wayward phosphotransferase in this lysosomal storage disorder, Kornfeld and his colleagues are investigating what goes wrong that allows it to escape the Golgi.
“We think there must be some protein in the cell that recognizes phosphotransferase when it gets to the end of the Golgi, binds it and takes it back,” said Kornfeld. “Now we’re trying to understand how that works.”
(Source: news.wustl.edu)
Researchers provide standardized nomenclature for the architecture of insect brains
When you’re talking about something as complex as the brain, the task isn’t any easier if the vocabulary being used is just as complex. An international collaboration of neuroscientists has not only tripled the number of identified brain structures, but created a simple lexicon to talk about them, which will be enormously helpful for future research on brain function and disease.
Nick Strausfeld and Linda Restifo, both professors in the Department of Neuroscience at the University of Arizona, worked with colleagues in Japan who led the project, and colleagues in Germany and in the UK to produce a comprehensive atlas of neuroanatomical centers and computational centers of the insect brain. In the process, the team identified many previously unknown structures. By providing the research community with a unified system of terminology, they set the stage for a systematic effort to elucidate brain structures and functions that carry over to functions of the human brain.
An article about the work appears in the scientific journal Neuron, regarded by many as one of the flagship publications of neuroscience; the online version includes an 80-page data supplement. The data will be publicly available within 6 months and include hundreds of images and 3-D video animations – amounting to an invaluable resource that will enable neuroscientists to work more efficiently, compare their results and obtain more meaningful interpretations.
"This effort provides a three-dimensional road map for describing structures for all insect brains, and enables comparisons with other arthropods," said Strausfeld, director of the UA Center for Insect Science. "It has huge value in describing network relationships between computational centers in the brain."
Study reveals workings of working memory
Keep this in mind: Scientists say they’ve learned how your brain plucks information out of working memory when you decide to act.
Say you’re a busy mom trying to wrap up a work call now that you’ve arrived home. While you converse on your Bluetooth headset, one kid begs for an unspecified snack, another asks where his homework project has gone, and just then an urgent e-mail from your boss buzzes the phone in your purse. During the call’s last few minutes these urgent requests — snack, homework, boss — wait in your working memory. When you hang up, you’ll pick one and act.
When you do that, according to Brown University psychology researchers whose findings appear in the journal Neuron, you’ll employ brain circuitry that links a specific chunk of the striatum called the caudate and a chunk of the prefrontal cortex centered on the dorsal anterior premotor cortex. Selecting from working memory, it turns out, uses similar circuits to those involved in planning motion.
In lab experiments with 22 adult volunteers, the researchers used magnetic resonance imaging to track brain activity during a carefully designed working memory task. They also measured how quickly the subjects could choose from working memory — a phenomenon the scientists called “output gating.”
“In the immediacy of what we’re doing we have this small working memory capacity where we can hang on to a few things that are going to be useful in a few moments, and that’s where output gating is crucial,” said study senior author David Badre, professor of cognitive, linguistic, and psychological sciences at Brown.
From the perspective of cognition, said lead author and postdoctoral scholar Christopher Chatham, input gating — choosing what goes into working memory — and output gating allow people to maintain a course of action (e.g., finish that Bluetooth call) while being flexible enough to account for context in planning what’s next.
Of cognition and wingdings
In their experiments Badre, Chatham, and co-author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences, provided their volunteers with four different versions of a similar working memory task. The versions distinguished output gating from input gating so that the anatomical action observed in the MRI could reliably associate with output gating behavior.
In each round, volunteers saw a sequence of characters — either letters of the alphabet or wingdings (typographical symbols like stars and snowflakes). Before or after the sequence, the volunteers were also given a context cue in the form of a numeral that told them which kind of character would be relevant at end of the task (e.g., “1” might mean a wingding while “2” might mean a letter). The last step for volunteers was to select between groups of characters on the screen that included whichever contextually relevant character they had seen in the sequence (e.g., if the subject had seen a “1” and later a snowflake during the sequence, they should select the group that included a snowflake).
When the context numeral came first, say a “2,” volunteers would “input gate” only letters into their working memory. When it came time to make a selection, they’d simply “output gate” the correct letter from the letters in working memory. If the context came last, people would have to input gate everything they saw into working memory, making all the real thinking a matter of output gating. If the context cue came last, they would carry a higher load of characters in working memory. To address this disparity, the experimenters created two more conditions in which a global context indicator, “3,” required people to keep everything they saw in working memory whether it came before the sequence or after.
With this experimental design the researchers could measure performance and monitor brain activity with subjects who had distinct moments of input and output gating, regardless of the character load in working memory.
People accomplished the tasks with a range of speeds, which the researchers regarded as a proxy for the amount of cognitive work volunteers had to do. People were slowest in making a selection when they got the context cue last and then had to gate just one specific symbol out of memory (e.g., they saw the sequence, then saw a 1, and then had to choose the option with a wingding they had seen). People were fastest at making a selection when they were given the context first and then had to pick the one character of that kind that they saw (e.g., they saw a “2,” then the sequence in which only letters mattered, and then had to choose the option with a letter they had seen).
In analyzing the results, Chatham and his co-authors found that the caudate and the dorsal anterior premotor cortex, contributed distinctly to the reaction times they saw. These separate roles in the partnership agree with computational models of how the brain works.
“The division of labor that’s specifically posited by these computational models is one in which there is a basically a context being represented in the prefrontal cortex that determines the overall efficiency of going from stimulus to response – like a route,” Chatham said. “The striatum is involved in the actual gating of that flow of information,” he said, “like traffic lights along the route.”
So the cortex interprets the context, while the striatum implements the gating. When the context is unhelpfully general and the gating is very specific, for example, the task takes a lot of time.
The findings help advance studies of how cognition works in the brain and could help psychiatrists analyze behavior in people where those areas of the brain have been injured, the researchers said. It also highlights how similar brain circuits can execute different functions – motion and working memory gating.
Scientists identify the switch that says it’s time to sleep
The switch works by regulating the activity of a handful of sleep-promoting nerve cells, or neurons, in the brain. The neurons fire when we’re tired and need sleep, and dampen down when we’re fully rested.
‘When you’re tired, these neurons in the brain shout loud and they send you to sleep,’ says Professor Gero Miesenböck of Oxford University, in whose laboratory the new research was performed.
Although the research was carried out in fruit flies, or Drosophila, the scientists say the sleep mechanism is likely to be relevant to humans.
Dr Jeffrey Donlea, one of the lead authors of the study, explains: ‘There is a similar group of neurons in a region of the human brain. These neurons are also electrically active during sleep and, like the flies’ cells, are the targets of general anaesthetics that put us to sleep. It’s therefore likely that a molecular mechanism similar to the one we have discovered in flies also operates in humans.’
The researchers say that pinpointing the sleep switch might help us identify new targets for novel drugs – potentially to improve treatments for sleep disorders.
But there is much still to find out, and further research could give insight into the big unanswered question of why we need to sleep at all, they say.
‘The big question now is to figure out what internal signal the sleep switch responds to,’ says Dr Diogo Pimentel of Oxford University, the other lead author of the study. ‘What do these sleep-promoting cells monitor while we are awake?
‘If we knew what happens in the brain during waking that requires sleep to reset, we might get closer to solving the mystery of why all animals need to sleep.’
The findings are reported in the journal Neuron. The work of the Centre for Neural Circuits and Behaviour is funded by the Wellcome Trust and the Gatsby Charitable Foundation. This study was also supported by the UK Medical Research Council, the US National Institutes of Health, and the Human Frontier Science Program.
The body uses two mechanisms to regulate sleep. One is the body clock, which attunes humans and animals to the 24 hour cycle of day and night. The other mechanism is the sleep ‘homeostat’: a device in the brain that keeps track of your waking hours and puts you to sleep when you need to reset. This mechanism represents an internal nodding off point that is separate from external factors. When it is turned off or out of use, sleep deficits build up.
What makes us go to sleep at night is probably a combination of the two mechanisms,’ says Professor Miesenböck. ‘The body clock says it’s the right time, and the sleep switch has built up pressure during a long waking day.’
The work in fruit flies allowed the critical part of the sleep switch to be discovered. ‘We discovered mutant flies that couldn’t catch up on their lost sleep after they had been kept awake all night,’ says Dr Jeffrey Donlea.
Flies stop moving when they go to sleep and require more disturbance to get them up. Sleep-deprived flies are prone to nodding off and are cognitively impaired – they have severe learning and memory deficits, much as sleep loss in humans leads to problems.
Professor Miesenböck says: ‘The sleep homeostat is similar to the thermostat in your home. A thermostat measures temperature and switches on the heating if it’s too cold. The sleep homeostat measures how long a fly has been awake and switches on a small group of specialized cells in the brain if necessary. It’s the electrical output of these nerve cells that puts the fly to sleep.’
In the mutant flies, the researchers were able to show a key molecular component of the electrical activity switch is broken and the sleep-inducing neurons are always off, causing insomnia.
(Source: ox.ac.uk)
Scientists identify new Huntington disease pathway
An international group of researchers has identified a major new pathway thought to be involved in the development of Huntington disease. The findings, published in the Proceedings of the National Academy of Sciences journal, could eventually lead to new treatments for the disease, which currently has no cure.
Scientists at the BC Cancer Agency Research Centre and the Centre for Molecular Medicine and Therapeutics in Vancouver, Canada, and the MRC Toxicology Unit in Leicester, UK, studied mice and human tissue and found that the HACE1 gene is essential for mopping up toxic molecules during periods of oxidative stress, where harmful ‘reactive oxygen species’ build up in the cell.
Oxidative stress is thought to be involved in the development of a number of diseases including cancer and neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. Therefore finding out how this process occurs in the body is important for understanding the course of disease.
The body has evolved highly effective defence mechanisms that sense and respond to oxidative stress to protect the cells from damage. One of these protective mechanisms is controlled by a molecule called NRF2 which springs into action and switches on the production of proteins and enzymes that detoxify the cell.
In this study, scientists found that the HACE1 also plays a vital role in this detoxification process, by activating NRF2. The authors believe that this mechanism goes wrong in Huntington’s disease, leading to gradual destruction of nerve cells in the brain.
Lead author Dr Barak Rotblat, of the MRC Toxicology Unit, said:
“One of the early observations was that enhanced HACE1 expression rescued cells from mutant Huntingtin (the mutant protein that is responsible for Huntington disease) toxicity. We knew then that we had to figure out how HACE1 can protect these cells.
“Our evidence points towards a previously unknown role of HACE1 in Huntington disease and possibly other forms of neurodegeneration. It’s very early days, but if we were able to find a way to boost this pathway, we might be able to develop a treatment that halts, or even reverses progression of Huntington disease.”
HACE1 is already known to play a protective role against tumour formation, but its role in neurodegeneration has not been investigated before.
Dr Poul Sorensen, the senior author of the work from the BC Cancer Agency Research Centre and a Professor at the University of British Columbia, said:
“This is a glowing example of how work in one field, namely childhood cancers, where we first identified the HACE1 gene, has applications to a completely different disease, Huntington disease”.
In this study, researchers looked at mice with and without the HACE1 gene and found that those without the gene had more oxidative stress in the brain, and their response to this was impaired. Depleting HACE1 in cells also resulted in reduced NRF2 activity, leading to lower tolerance against oxidative stress triggers.
The scientists also looked at human brain samples from Huntington disease patients and found a striking reduction of HACE1 levels in the striatum – the area of the brain where the disease develops and is most damaged.
Finally, they looked at HACE1 in a cellular model of Huntington disease. They found that upping expression of the gene in nerve precursor cells protected them against oxidative stress.
(Source: mrc.ac.uk)
The brains of jazz musicians engrossed in spontaneous, improvisational musical conversation showed robust activation of brain areas traditionally associated with spoken language and syntax, which are used to interpret the structure of phrases and sentences. But this musical conversation shut down brain areas linked to semantics - those that process the meaning of spoken language, according to results of a study by Johns Hopkins researchers.
The study used functional magnetic resonance imaging (fMRI) to track the brain activity of jazz musicians in the act of “trading fours,” a process in which musicians participate in spontaneous back and forth instrumental exchanges, usually four bars in duration. The musicians introduce new melodies in response to each other’s musical ideas, elaborating and modifying them over the course of a performance.
The results of the study suggest that the brain regions that process syntax aren’t limited to spoken language, according to Charles Limb, M.D., an associate professor in the Department of Otolaryngology-Head and Neck Surgery at the Johns Hopkins University School of Medicine. Rather, he says, the brain uses the syntactic areas to process communication in general, whether through language or through music.
Limb, who is himself a musician and holds a faculty appointment at the Peabody Conservatory, says the work sheds important new light on the complex relationship between music and language.
"Until now, studies of how the brain processes auditory communication between two individuals have been done only in the context of spoken language," says Limb, the senior author of a report on the work that appears online Feb. 19 in the journal PLOS ONE. “But looking at jazz lets us investigate the neurological basis of interactive, musical communication as it occurs outside of spoken language.
"We’ve shown in this study that there is a fundamental difference between how meaning is processed by the brain for music and language. Specifically, it’s syntactic and not semantic processing that is key to this type of musical communication. Meanwhile, conventional notions of semantics may not apply to musical processing by the brain."
To study the response of the brain to improvisational musical conversation between musicians, the Johns Hopkins researchers recruited 11 men aged 25 to 56 who were highly proficient in jazz piano performance. During each 10-minute session of trading fours, one musician lay on his back inside the MRI machine with a plastic piano keyboard resting on his lap while his legs were elevated with a cushion. A pair of mirrors was placed so the musician could look directly up while in the MRI machine and see the placement of his fingers on the keyboard. The keyboard was specially constructed so it did not have metal parts that would be attracted to the large magnet in the fMRI.
The improvisation between the musicians activated areas of the brain linked to syntactic processing for language, called the inferior frontal gyrus and posterior superior temporal gyrus. In contrast, the musical exchange deactivated brain structures involved in semantic processing, called the angular gyrus and supramarginal gyrus.
"When two jazz musicians seem lost in thought while trading fours, they aren’t simply waiting for their turn to play," Limb says. "Instead, they are using the syntactic areas of their brain to process what they are hearing so they can respond by playing a new series of notes that hasn’t previously been composed or practiced."