Posts tagged motor cortex

Posts tagged motor cortex
Extraordinarily complex networks of circuits that transmit signals from the brain to the spinal cord control voluntary movements. Researchers have been challenged to identify the controlling circuits, but they lacked the tools needed to dissect, at the neural level, the way the brain produces voluntary movements.
Recently, Dr. John Martin, medical professor in City College’s Sophie Davis School of Biomedical Education, postdoctoral fellow Dr. Najet Serradi and other colleagues employed a sensitive genetic technique that eliminated a particular gene in the cerebral cortex and, in the process, changed the circuitry.
The team hypothesized that the corticospinal tract, which stretches from cerebral cortex to the spinal cord, is important for voluntary reaching movements, but not for more routine and stereotypic walking movements. “We reasoned that if we genetically altered the corticospinal tract we would affect voluntary reaching movements, but not walking.” Professor Martin said.
In genetically intact mice, corticospinal tract signals are transmitted from one side of the cerebral cortex to the opposite side of the spinal cord. Such mice reach with one arm, or the other – but not both arms together.
Professor Martin and colleagues used specially bred mice, i.e. knockout mice, with the gene EphA4 removed from the cerebral cortex. These mice reached with both forelimbs together, rather than with one. This happened because the genetic manipulation changed the circuit; it caused the signal to move to be transmitted from one side of the cerebral cortex to both sides of the spinal cord.
However, their stereotypic walking was unaffected. Professor Martin said this shows that while voluntary movements depend on the corticospinal tract walking depends on circuits in other parts of the brain and spinal cord, which are not affected by the gene manipulation.
The findings, he added, “etch away at the vexing problem of achieving a deeper understanding of how the brain functions in voluntary movement.” In addition greater knowledge of how voluntary circuits function could lead to new understanding of cerebral palsy, a condition in which the corticospinal tract is injured around the time of birth and people often make “mirror movements” of both arms when they intend to move only one, he said.
The research, which is funded by the National Institute of Neurological Diseases and Stroke, aims to understand the brain and spinal cord circuits for voluntary movement. Using similar genetic tools, his team hopes to further dissect the connections and functions of the corticospinal tract movement circuits in ways to restore movements after brain or spinal cord injury.
(Source: www1.cuny.edu)
Motor cortex shown to play active role in learning movement patterns
Skilled motor movements of the sort tennis players employ while serving a tennis ball or pianists use in playing a concerto, require precise interactions between the motor cortex and the rest of the brain. Neuroscientists had long assumed that the motor cortex functioned something like a piano keyboard.
"Every time you wanted to hear a specific note, there was a specific key to press," says Andrew Peters, a neurobiologist at UC San Diego’s Center for Neural Circuits and Behavior. "In other words, every specific movement of a muscle required the activation of specific cells in the motor cortex because the main job of the motor cortex was thought to be to listen to the rest of the cortex and press the keys it’s directed to press."
But in a study published in this week’s advance online publication of the journal Nature, Peters, the first author of the paper, and his colleagues found that the motor cortex itself plays an active role in learning new motor movements. In a series of experiments using mice, the researchers showed in detail how those movements are learned over time.
"Our finding that the relationship between body movements and the activity of the part of the cortex closest to the muscles is profoundly plastic and shaped by learning provides a better picture of this process," says Takaki Komiyama, an assistant professor of biology at UC San Diego who headed the research team. "That’s important, because elucidating brain plasticity during learning could lead to new avenues for treating learning and movement disorders, including Parkinson’s disease."
With Simon Chen, another UC San Diego neurobiologist, the researchers monitored the activity of neurons in the motor cortex over a period of two weeks while mice learned to press a lever in a specific way with their front limbs to receive a reward.
"What we saw was that during learning, different patterns of activity—which cells are active, when they’re active—were evident in the motor cortex," says Peters. "This ends up translating to different patterns of activity even for similar movements. Once the animal has learned the movement, similar movements are then accompanied by consistent activity. This consistent activity moreover is totally new to the animal: it wasn’t used early in learning even with movements that were similar to the later movement."
"Early on," Peters says, "the animals will occasionally make movements that look like the expert movements they make after learning. The patterns of brain activity that accompany those similar early and late movements are actually completely different though. Over the course of learning, the animal generates a whole new set of activity in the motor cortex to make that movement. In the piano keyboard analogy, that’s like using one key to make a note early on, but a different key to make the same note later."

Researchers find hand to mouth movement in humans likely hard-wired
A team of researchers in France has found evidence that suggests that human hand-to-mouth actions are hard-wired into the brain. In their paper published in Proceedings of the National Academy of Sciences, the researchers describe an experiment they conducted on adults undergoing brain surgery and why what they found could have profound implications on human brain development theories.
Johns Hopkins researchers report that people with chronic insomnia show more plasticity and activity than good sleepers in the part of the brain that controls movement.
"Insomnia is not a nighttime disorder," says study leader Rachel E. Salas, M.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. "It’s a 24-hour brain condition, like a light switch that is always on. Our research adds information about differences in the brain associated with it."

Salas and her team, reporting in the March issue of the journal Sleep, found that the motor cortex in those with chronic insomnia was more adaptable to change - more plastic - than in a group of good sleepers. They also found more “excitability” among neurons in the same region of the brain among those with chronic insomnia, adding evidence to the notion that insomniacs are in a constant state of heightened information processing that may interfere with sleep.
Researchers say they hope their study opens the door to better diagnosis and treatment of the most common and often intractable sleep disorder that affects an estimated 15 percent of the United States population.
To conduct the study, Salas and her colleagues from the Department of Psychiatry and Behavioral Sciences and the Department of Physical Medicine and Rehabilitation used transcranial magnetic stimulation (TMS), which painlessly and noninvasively delivers electromagnetic currents to precise locations in the brain and can temporarily and safely disrupt the function of the targeted area. TMS is approved by the U.S. Food and Drug Administration to treat some patients with depression by stimulating nerve cells in the region of the brain involved in mood control.
The study included 28 adult participants - 18 who suffered from insomnia for a year or more and 10 considered good sleepers with no reports of trouble sleeping. Each participant was outfitted with electrodes on their dominant thumb as well as an accelerometer to measure the speed and direction of the thumb.
The researchers then gave each subject 65 electrical pulses using TMS, stimulating areas of the motor cortex and watching for involuntary thumb movements linked to the stimulation. Subsequently, the researchers trained each participant for 30 minutes, teaching them to move their thumb in the opposite direction of the original involuntary movement. They then introduced the electrical pulses once again.
The idea was to measure the extent to which participants’ brains could learn to move their thumbs involuntarily in the newly trained direction. The more the thumb was able to move in the new direction, the more likely their motor cortexes could be identified as more plastic.
Because lack of sleep at night has been linked to decreased memory and concentration during the day, Salas and her colleagues suspected that the brains of good sleepers could be more easily retrained. The results, however, were the opposite. The researchers found much more plasticity in the brains of those with chronic insomnia.
Salas says the origins of increased plasticity in insomniacs are unclear, and it is not known whether the increase is the cause of insomnia. It is also unknown whether this increased plasticity is beneficial, the source of the problem or part of a compensatory mechanism to address the consequences of sleep deprivation associated with chronic insomnia. Patients with chronic phantom pain after limb amputation and with dystonia, a neurological movement disorder in which sustained muscle contractions cause twisting and repetitive movements, also have increased brain plasticity in the motor cortex, but to detrimental effect.
Salas says it is possible that the dysregulation of arousal described in chronic insomnia - increased metabolism, increased cortisol levels, constant worrying - might be linked to increased plasticity in some way. Diagnosing insomnia is solely based on what the patient reports to the provider; there is no objective test. Neither is there a single treatment that works for all people with insomnia. Treatment can be a hit or miss in many patients, Salas says.
She says this study shows that TMS may be able to play a role in diagnosing insomnia, and more importantly, she says, potentially prove to be a treatment for insomnia, perhaps through reducing excitability.
(Source: hopkinsmedicine.org)
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.”

Stanford researchers may have solved a riddle about the inner workings of the brain, which consists of billions of neurons, organized into many different regions, with each region primarily responsible for different tasks.
The various regions of the brain often work independently, relying on the neurons inside that region to do their work. At other times, however, two regions must cooperate to accomplish the task at hand. The riddle is this: what mechanism allows two brain regions to communicate when they need to cooperate yet avoid interfering with one another when they must work alone?
In a paper published today in Nature Neuroscience, a team led by Stanford electrical engineering professor Krishna Shenoy reveals a previously unknown process that helps two brain regions cooperate when joint action is required to perform a task.
“This is among the first mechanisms reported in the literature for letting brain areas process information continuously but only communicate what they need to,” said Matthew T. Kaufman, who was a postdoctoral scholar in the Shenoy lab when he co-authored the paper.
(Source: engineering.stanford.edu)
Motor Excitability predicts Working Memory
Humans with a high motor excitability have a better working memory than humans with a low excitability. This was shown in a study conducted by scientists from the Transfacultary Research Platform at the University of Basel. By measuring the motor excitability, conclusions can be drawn as to the general cortical excitability – as well as to cognitive performance.
Working memory allows the temporary storage of information such as memorizing a phone number for a short period of time. Studies in animals have shown that working memory processes among others depend on the excitability of neurons in the prefrontal cortex. Moreover, there is evidence that motor neuronal excitability might be related to the neuronal excitability of other cortical regions. Researchers from the Psychiatric University Clinics (UPK Basel) and the Faculty of Psychology in Basel have now studied if the excitability of the motor cortex correlates with working memory performance– results were positive.
«The motor cortical excitability can be easily studied with transcranial magnetic stimulation», says Nathalie Schicktanz, doctoral student and first author of the study. During this procedure, electromagnetic impulses with increasing intensity are applied over the motor cortex. For subjects with high motor excitability already weak impulses are sufficient to trigger certain muscles – such as those of the hand – to show a visible twitch.
Conclusions for other cortical regions
In the present study, that included 188 healthy young subjects, the scientists were able to show that subjects with a high motor excitability had increased working memory performance as compared to subjects with a low excitability. «By measuring the excitability of the motor cortex, conclusions can be drawn as to the excitability of other cortical areas», says Schicktanz.
«The findings help us to understand the importance of neuronal excitability for cognitive processes in humans», adds Dr. Kyrill Schwegler, co-author of the study. The results might also have important clinical implications, as working memory deficits are a component of many neuropsychiatric disorders, such as schizophrenia or attention deficit hyperactivity disorder. In a next step, the scientists plan to study the relation between neuronal excitability and memory on a molecular level.
The study is part of a project lead by Prof. Dominique de Quervain and Prof. Andreas Papassotiropoulos. The project uses transcranial magnetic stimulation to study the cognitive functions in humans. The goal is to identify the neurobiological and molecular mechanisms of human memory.
Baby brains are tuned to the specific actions of others
Imitation may be the sincerest form of flattery for adults, but for babies it’s their foremost tool for learning. As renowned people-watchers, babies often observe others demonstrate how to do things and then copy those body movements. It’s how little ones know, usually without explicit instructions, to hold a toy phone to the ear or guide a spoon to the mouth.
Now researchers from the University of Washington and Temple University have found the first evidence revealing a key aspect of the brain processing that occurs in babies to allow this learning by observation.
The findings, published online Oct. 30 by PLOS ONE, are the first to show that babies’ brains showed specific activation patterns when an adult performed a task with different parts of her body. When 14-month-old babies simply watched an adult use her hand to touch a toy, the hand area of the baby’s brain lit up. When another group of infants watched an adult touch the toy using only her foot, the foot area of the baby’s brain showed more activity.
"Babies are exquisitely careful people-watchers, and they’re primed to learn from others," said Andrew Meltzoff, co-author and co-director of the UW Institute for Learning & Brain Sciences. "And now we see that when babies watch someone else, it activates their own brains. This study is a first step in understanding the neuroscience of how babies learn through imitation."
The study took advantage of how the brain is organized. The sensory and motor area of the cortex, the outer portion of the brain known for its creased appearance, is arranged by body part with each area of the body represented in identifiable neural real estate. Prick your finger, stick out your tongue, or kick a ball and distinct areas of the brain light up according to a somatotopic map.
Other studies show that adults show this somatotopic brain activation while watching someone else use different body parts, suggesting that adults understand the actions of others in relation to their own bodies. The researchers wondered whether the same would be true in babies.
The 70 infants in the study wore electroencephalogram, or EEG, caps with embedded sensors that detected brain activity in the regions of the cortex that respond to movement or touch of the feet and hands. Sitting on a parent’s lap, each baby watched as an experimenter touched a toy placed on a low table between the baby and the experimenter.
The toy had a clear plastic dome and was mounted on a sturdy base. When the experimenter pressed the dome with her hand or foot, music played and confetti in the dome spun. The experimenter repeated the action – taking breaks after every four presses – until the baby lost interest.
"Our findings show that when babies see others produce actions with a particular body part, their brains are activated in a corresponding way," said Joni Saby, lead author and a psychology graduate student at Temple University in Philadelphia. "This mapping may facilitate imitation and could play a role in the baby’s ability to then produce the same actions themselves."
One of the basics for babies to learn is how to copy what they see adults do. In other words, they must first know that it is indeed their hand and not their foot, mouth or other body part that is needed.
The new study shows that babies’ brains are organized in a somatotopic way that helps crack the interpersonal code. The connection between doing and seeing actions maps hand to hand, foot to foot, all before they can name those body parts through language.
"The reason this is exciting is that it gives insight into a crucial aspect of imitation," said co-author Peter Marshall, an associate psychology professor at Temple University. "To imitate the action of another person, babies first need to register what body part the other person used. Our findings suggest that babies do this in a particular way by mapping the actions of the other person onto their own body."
Meltzoff added, “The neural system of babies directly connects them to other people, which jump-starts imitation and social-emotional connectedness and bonding. Babies look at you and see themselves.”
Rats! Humans and rodents face their errors
What happens when the brain recognizes an error? A new study shows that the brains of humans and rats adapt in a similar way to errors by using low-frequency brainwaves in the medial frontal cortex to synchronize neurons in the motor cortex. The finding could be important in studies of “adaptive control” like obsessive compulsive disorder, ADHD, and Parkinson’s.
People and rats may think alike when they’ve made a mistake and are trying to adjust their thinking.
That’s the conclusion of a study published online Oct. 20 in Nature Neuroscience that tracked specific similarities in how human and rodent subjects adapted to errors as they performed a simple time estimation task. When members of either species made a mistake in the trials, electrode recordings showed that they employed low-frequency brainwaves in the medial frontal cortex (MFC) of the brain to synchronize neurons in their motor cortex. That action correlated with subsequent performance improvements on the task.
“These findings suggest that neuronal activity in the MFC encodes information that is involved in monitoring performance and could influence the control of response adjustments by the motor cortex,” wrote the authors, who performed the research at Brown University and Yale University.
The importance of the findings extends beyond a basic understanding of cognition, because they suggest that rat models could be a useful analog for humans in studies of how such “adaptive control” neural mechanics are compromised in psychiatric diseases.
“With this rat model of adaptive control, we are now able to examine whether novel drugs or other treatment procedures boost the integrity of this system,” said James Cavanagh, co-lead author of the paper who was at Brown when the research was done and has since become assistant professor of psychology at the University of New Mexico. “This may have clear translational potential for treating psychiatric diseases such as obsessive compulsive disorder, depression, attention deficit hyperactivity disorder, Parkinson’s disease and schizophrenia.”
To conduct the study, the researchers measured external brainwaves of human and rodent subjects after both erroneous and accurate performance on the time estimation task. They also measured the activity of individual neurons in the MFC and motor cortex of the rats in both post-error and post-correct circumstances.
The scientists also gave the rats a drug that blocked activity of the MFC. What they saw in those rats compared to rats who didn’t get the drug, was that the low-frequency waves did not occur in the motor cortex, neurons there did not fire coherently and the rats did not alter their subsequent behavior on the task.
Although the researchers were able to study the cognitive mechanisms in the rats in more detail than in humans, the direct parallels they saw in the neural mechanics of adaptive control were significant.
“Low-frequency oscillations facilitate synchronization among brain networks for representing and exerting adaptive control, including top-down regulation of behavior in the mammalian brain,” they wrote.

Brain Wiring Quiets the Voice Inside Your Head
Researchers find nerve circuits connecting motion and hearing
During a normal conversation, your brain is constantly adjusting the volume to soften the sound of your own voice and boost the voices of others in the room. This ability to distinguish between the sounds generated from your own movements and those coming from the outside world is important not only for catching up on water cooler gossip, but also for learning how to speak or play a musical instrument.
Now, researchers have developed the first diagram of the brain circuitry that enables this complex interplay between the motor system and the auditory system to occur.
The research, which appears Sept. 4 in The Journal of Neuroscience, could lend insight into schizophrenia and mood disorders that arise when this circuitry goes awry and individuals hear voices other people do not hear.
"Our finding is important because it provides the blueprint for understanding how the brain communicates with itself, and how that communication can break down to cause disease," said Richard Mooney, Ph.D., senior author of the study and professor of neurobiology at Duke University School of Medicine. "Normally, motor regions would warn auditory regions that they are making a command to speak, so be prepared for a sound. But in psychosis, you can no longer distinguish between the activity in your motor system and somebody else’s, and you think the sounds coming from within your own brain are external."
Researchers have long surmised that the neuronal circuitry conveying movement — to voice an opinion or hit a piano key — also feeds into the wiring that senses sound. But the nature of the nerve cells that provided that input, and how they functionally interacted to help the brain anticipate the impending sound, was not known.
In this study, Mooney used a technology created by Fan Wang, Ph.D., associate professor of cell biology at Duke, to trace all of the inputs into the auditory cortex — the sound-interpreting region of the brain. Though the researchers found that a number of different areas of the brain fed into the auditory cortex, they were most interested in one region called the secondary motor cortex, or M2, because it is responsible for sending motor signals directly into the brain stem and the spinal cord.
"That suggests these neurons are providing a copy of the motor command directly to the auditory system," said David M. Schneider, Ph.D., co-lead author of the study and a postdoctoral fellow in Mooney’s lab. "In other words,they send a signal that says âmove,â but they also send a signal to the auditory system saying ‘I am going to move.’"
Having discovered this connection, the researchers then explored what type of influence this interaction was having on auditory processing or hearing. They took slices of brain tissue from mice and specifically manipulated the neurons that led from the M2 region to the auditory cortex. The researchers found that stimulating those neurons actually dampened the activity of the auditory cortex.
"It jibed nicely with our expectations," said Anders Nelson, co-lead author of the study and a graduate student in Mooney’s lab. "It is the brain’s way of muting or suppressing the sounds that come from our own actions."
Finally, the researchers tested this circuitry in live animals, artificially turning on the motor neurons in anesthetized mice and then looking to see how the auditory cortex responded. Mice usually sing to each other through a kind of song called ultrasonic vocalizations, which are too high-pitched for a human to hear. The researchers played back these ultrasonic vocalizations to the mice after they had activated the motor cortex and found that the neurons became much less responsive to the sounds.
"It appears that the functional role that these neurons play on hearing is they make sounds we generate seem quieter," said Mooney. "The question we now want to know is if this is the mechanism that is being used when an animal is actually moving. That is the missing link, and the subject of our ongoing experiments."
Once the researchers have pinned down the basics of the circuitry, they could begin to investigate whether altering this circuitry could induce auditory hallucinations or perhaps even take them away in models of schizophrenia.