Neuroscience

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Posts tagged basal ganglia

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Dreams: Full of meaning or a reflex of the brain?

It’s a question that has long fascinated and flummoxed those who study human behavior: From whence comes the impulse to dream? Are dreams generated from the brain’s “top” — the high-flying cortical structures that allow us to reason, perceive, act and remember? Or do they come from the brain’s “bottom” — the unheralded brainstem, which quietly oversees such basic bodily functions as respiration, heart rate, salivation and temperature control?

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At stake is what to make of the funny, sexual, scary and just plain bizarre mental scenarios that play themselves out in our heads while we sleep. Are our subconsious fantasies coming up for a breath of air, as Sigmund Freud believed? Is our brain consolidating lessons learned and pitching out unneeded data, as neuroscientists suggest? Or are dreams no more meaningful than a spontaneous run of erratic heartbeats, a hot flash, or the frisson we feel at the sight of an attractive passer-by?

A study published this week in the journal Brain suggests that the impulse to dream may be little more than a tickle sent up from the brainstem to the brain’s sensory cortex.

The full dream experience — the complex scenarios, the feelings of fear, delight or longing — may require the further input of the brain’s higher-order cortical areas, the new research suggests. But even people with grievous injury to the brain’s prime motivational machinery are capable of dreams, the study found.

The latest research looked for sleep-time “mentation” — thoughts, essentially — in a small group of very unusual patients. These patients — 13 in all — had suffered damage within their brains’ limbic system, the seat of our basic desires and motivations — for sex, for food, for pleasurable sensations brought on by drugs and friendship and whatever else turns us on.

As a result of that damage, they had a neuropsychological syndrome called auto-activation deficit, or AAD: Even while fully conscious, they could sit completely idle and mute for hours if they were not prodded to action or speech by caregivers. In fact, they were more than unmotivated to do anything; when asked about their thoughts, they would frequently report that their mind was completely blank. When prompted, they could often do math, sing a song or conjure up memories. But left on their own, these patients might have no spontaneous thoughts at all.

Do these people dream? The answer might suggest the answer to the question of where dreams come from.

Indeed, they do dream — or at least some of them did, in an experiment that compared the nighttime mentations of normal, healthy subjects with subjects who suffered from AAD. When awakened from rapid eye movement (REM) sleep — the sleep stage at which dreams are thought to be most common and complex — four of the patients with AAD — 31% of them — reported mentations.

That was a lot less dreaming than was happening in the healthy subjects, 92% of whom reported dreams — and much more colorful and bizarre ones — when they were awakened from REM sleep.

In the AAD patients, the dreams were rarer, shorter and less complex: they said they dreamed of things like shaving, taking a walk or seeing a relative. But even these rudimentary dreams cast them in situations that, in a conscious state, they were unlikely to think of unprompted.

That these inert patients could generate dreams was a “most unexpected result,” said the study’s authors, a team of French neurologists, neuroscientists and sleep specialists based in several institutes in Paris. It supports the hypothesis that “dreams are generated through bottom-up processes,” they concluded.

The “top-down theory” — that dreams originate from the brain’s higher-order cortex, the place from which imagination springs — “is not supported here,” the authors said, “as patients with AAD who have a mental emptiness and no imagination during wakefulness do report some dream mentations upon emerging from sleep.”

Of course, the dreams of healthy subjects may be enbellished by input from the cortical areas that are the seats of perception, memory, emotion and reason, the authors said: That is demonstrated by the vastly richer dreams described by normal subjects.

A lot of dream research in humans has been based on subjects with bizarre damage to the brain. People who have had frontal lobotomies, for instance, report an abrupt cessation of dream activity — an observation that had rallied the top-down view of the dream impulse.

It’s an imperfect method of research, since such subjects are rare and no two have exactly the same injuries. So, while the rest of us dream away unbothered, this intriguing debate is likely to remain open for some time to come.

(Source: Los Angeles Times)

Filed under auto-activation deficit sleep dream basal ganglia REM sleep neuroscience psychology science

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Deconstructing motor skills
Hitting the perfect tennis serve requires hours and hours of practice, but for scientists who study complex motor behaviors, there always has been a large unanswered question — what is the brain learning from those hours spent on the court? Is it simply the timing required to hit the perfect serve, or is it the precise path along which to move the hand?
The answer, Harvard researchers say, is both — but in separate circuits.
Bence Ölveczky, the John L. Loeb Associate Professor of the Natural Sciences, has found that the brain uses two largely independent neural circuits to learn the temporal and spatial aspects of a motor skill. The study is described in a Sept. 26 paper in Neuron.
“What we’re studying is the structure of motor-skill learning,” Ölveczky said. “What we were able to show is that the brain divides something that’s complex into modules — in this case for timing and for motor implementation — as a way to take advantage of the hierarchical structure of the motor system, and it imprints learning at the different levels independently.”
To tease out how those independent circuits operate, Ölveczky and his colleagues turned to a creature well-known for its ability to learn — the zebra finch. The tiny birds are regularly used in studies of learning because each male learns to sing a unique song from its father.
In a series of experiments, Ölveczky’s team used traditional conditioning techniques to change the timing of a bird’s song by speeding up or slowing down certain “syllables” in the song. They could also change which vocal muscles were activated and have the bird sing at a higher or lower pitch.
“But when you change the pitch of a syllable, the duration doesn’t change, and when you change the duration the pitch doesn’t change,” Ölveczky said. “It appears the neural circuits for the two features are separate.”
Additional evidence that the circuits for learning motor implementation and timing are distinct came when researchers lesioned the basal ganglia of the birds — the region of the brain long thought to play a critical role in song learning.
“The thinking had been that there was one circuit for song-learning in general,” Ölveczky said. “We found that if we lesioned the basal ganglia and repeated the pitch-shift experiment, the bird could no longer use the information it got from our feedback to change its behavior — in other words, it couldn’t learn.”
Experiments aimed at changing the birds’ timing, however, were just as effective, suggesting two separate learning circuits — with only one involving the basal ganglia.
Such independence and modularity is critical, Ölveczky said, because it allows different features of a behavior to be modified independently if circumstances change. Parallel learning of different features can also speed up the learning process and enable the flexibility we see in birdsong and many human motor skills.
“If you learn something — it could be your tennis serve, or it could be any behavior — and you need to slow it down or speed it up to fit some new contingency, you don’t have to completely re-learn the whole thing, you can just change the timing, and everything else will remain exactly the same.
“In fact, ‘slow practice,’ a technique used by many piano and dance teachers, makes good use of this modularity,” Ölveczky said. “Students are first taught to perform the movements of a piece slowly. Once they have learned it, all they need to do is get the timing right. The technique works because the two processes — motor implementation and timing — do not interfere with each other.”
The hope among researchers, Ölveczky said, is that a better understanding of how birds learn complex motor tasks such as singing unique songs will help shed new light on the neural underpinnings of learning in humans.
“For us, this is inspiration to look at similar types of questions in mammals,” he said. “The flexibility with which we can alter the spatial and temporal structure of our motor output is similar to songbirds, but our understanding of how the mammalian brain implements the underlying learning process is not anywhere near as advanced as for songbirds. The intriguing parallels in both circuitry and behavior, however, suggest a general principle of how the brain parses the motor skill learning process.”

Deconstructing motor skills

Hitting the perfect tennis serve requires hours and hours of practice, but for scientists who study complex motor behaviors, there always has been a large unanswered question — what is the brain learning from those hours spent on the court? Is it simply the timing required to hit the perfect serve, or is it the precise path along which to move the hand?

The answer, Harvard researchers say, is both — but in separate circuits.

Bence Ölveczky, the John L. Loeb Associate Professor of the Natural Sciences, has found that the brain uses two largely independent neural circuits to learn the temporal and spatial aspects of a motor skill. The study is described in a Sept. 26 paper in Neuron.

“What we’re studying is the structure of motor-skill learning,” Ölveczky said. “What we were able to show is that the brain divides something that’s complex into modules — in this case for timing and for motor implementation — as a way to take advantage of the hierarchical structure of the motor system, and it imprints learning at the different levels independently.”

To tease out how those independent circuits operate, Ölveczky and his colleagues turned to a creature well-known for its ability to learn — the zebra finch. The tiny birds are regularly used in studies of learning because each male learns to sing a unique song from its father.

In a series of experiments, Ölveczky’s team used traditional conditioning techniques to change the timing of a bird’s song by speeding up or slowing down certain “syllables” in the song. They could also change which vocal muscles were activated and have the bird sing at a higher or lower pitch.

“But when you change the pitch of a syllable, the duration doesn’t change, and when you change the duration the pitch doesn’t change,” Ölveczky said. “It appears the neural circuits for the two features are separate.”

Additional evidence that the circuits for learning motor implementation and timing are distinct came when researchers lesioned the basal ganglia of the birds — the region of the brain long thought to play a critical role in song learning.

“The thinking had been that there was one circuit for song-learning in general,” Ölveczky said. “We found that if we lesioned the basal ganglia and repeated the pitch-shift experiment, the bird could no longer use the information it got from our feedback to change its behavior — in other words, it couldn’t learn.”

Experiments aimed at changing the birds’ timing, however, were just as effective, suggesting two separate learning circuits — with only one involving the basal ganglia.

Such independence and modularity is critical, Ölveczky said, because it allows different features of a behavior to be modified independently if circumstances change. Parallel learning of different features can also speed up the learning process and enable the flexibility we see in birdsong and many human motor skills.

“If you learn something — it could be your tennis serve, or it could be any behavior — and you need to slow it down or speed it up to fit some new contingency, you don’t have to completely re-learn the whole thing, you can just change the timing, and everything else will remain exactly the same.

“In fact, ‘slow practice,’ a technique used by many piano and dance teachers, makes good use of this modularity,” Ölveczky said. “Students are first taught to perform the movements of a piece slowly. Once they have learned it, all they need to do is get the timing right. The technique works because the two processes — motor implementation and timing — do not interfere with each other.”

The hope among researchers, Ölveczky said, is that a better understanding of how birds learn complex motor tasks such as singing unique songs will help shed new light on the neural underpinnings of learning in humans.

“For us, this is inspiration to look at similar types of questions in mammals,” he said. “The flexibility with which we can alter the spatial and temporal structure of our motor output is similar to songbirds, but our understanding of how the mammalian brain implements the underlying learning process is not anywhere near as advanced as for songbirds. The intriguing parallels in both circuitry and behavior, however, suggest a general principle of how the brain parses the motor skill learning process.”

Filed under learning motor skills basal ganglia premotor cortex nervous system neuroscience science

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Brain may rely on computer-like mechanism to make sense of novel situations

Our brains give us the remarkable ability to make sense of situations we’ve never encountered before—a familiar person in an unfamiliar place, for example, or a coworker in a different job role—but the mechanism our brains use to accomplish this has been a longstanding mystery of neuroscience.

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Now, researchers at the University of Colorado Boulder have demonstrated that our brains could process these new situations by relying on a method similar to the “pointer” system used by computers. “Pointers” are used to tell a computer where to look for information stored elsewhere in the system to replace a variable.

For the study, published today in the Proceedings of the National Academy of Sciences, the research team relied on sentences with words used in unique ways to test the brain’s ability to understand the role familiar words play in a sentence even when those words are used in unfamiliar, and even nonsensical, ways. 

For example, in the sentence, “I want to desk you,” we understand the word “desk” is being used as a verb even though our past experience with the word “desk” is as a noun.

“The fact that you understand that the sentence is grammatically well formed means you can process these completely novel inputs,” said Randall O’Reilly, a professor in CU-Boulder’s Department of Psychology and Neuroscience and co-author of the study. “But in the past when we’ve tried to get computer models of a brain to do that, we haven’t been successful.”

This shows that human brains are able to understand the sentence as a structure with variables—a subject, a verb and often, an object—and that the brain can assign a wide variety of words to those variables and still understand the sentence structure. But the way the brain does this has not been understood.

Computers routinely complete similar tasks. In computer science, for example, a computer program could create an email form letter that has a pointer in the greeting line. The pointer would then draw the name information for each individual recipient into the greeting being sent to that person.

In the new study, led by Trenton Kriete, a postdoctoral researcher in O’Reilly’s lab, the scientists show that the connections in the brain between the prefrontal cortex and the basal ganglia could play a similar role to the pointers used in computer science. The researchers added new information about how the connections between those two regions of the brain could work into their model.

The result was that the model could be trained to understand simple sentences using a select group of words. After the training period, the researchers fed the model new sentences using familiar words in novel ways and found that the model could still comprehend the sentence structure.

While the results show that a pointer-like system could be at play in the brain, the function is not identical to the system used in computer science, the scientists said. It’s similar to comparing an airplane’s wing and a bird’s wing, O’Reilly said. They’re both used for flying but they work differently.

In the brain, for example, the pointer-like system must still be learned. The brain has to be trained, in this case, to understand sentences while a computer can be programmed to understand sentences immediately.

“As your brain learns, it gets better and better at processing these novel kinds of information,” O’Reilly said.

(Source: colorado.edu)

Filed under basal ganglia prefrontal cortex cognitive processing psychology neuroscience science

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Dreaming is still possible even when the mind is blank

Isabelle Arnulf and colleagues from the Sleep Disorders Unit at the Université Pierre et Marie Curie (UPMC) have outlined case studies of patients with Auto-Activation Deficit who reported dreams when awakened from REM sleep – even when they demonstrated a mental blank during the daytime. This paper proves that even patients with Auto-Activation Disorder have the ability to dream and that it is the “bottom-up” process that causes the dream state.

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In a new paper for the neurology journal Brain, Arnulf et al compare the dream states of patients with Auto-Activation Deficit (AAD) with those of healthy, control patients. AAD is caused by bilateral damage to the basal ganglia and it is a neuro-physical syndrome characterized by a striking apathy, a lack of spontaneous activation of thought, and a loss of self-driven behaviour. AAD patients must be stimulated by their care-givers in order to take part in everyday tasks like standing up, eating, or drinking. If you were to ask an AAD patient: “what are you thinking?” they would report that they have no thoughts.

During sleep, the brain is operating on an exclusively internal basis. In REM sleep, the higher cortex areas are internally stimulated by the brainstem. When awakened, most normal subjects will remember some dreams that were associated with their previous sleep state, especially in REM sleep. Would the self-stimulation of the cortex by the brainstem be sufficient to stimulate spontaneous dreams during sleep in AAD patients?

Discovering the answer to this question would go some way to proving either the top-down or bottom-up theories of dreaming. The top-down theory stipulates that dreaming begins in higher cortex memory structures and then proceeds backwards as imagination develops during wakefulness. The bottom-up theory posits that the brainstem structures which elicit rapid eye movements and cortex activation during REM sleep result in the emotional, visual, sensory, and auditory elements of dreaming.

Thirteen patients with AAD agreed to participate in the study and record their dreams in dream diaries during the week leading up to the evaluation. These patients were compared with thirteen non-medicated, healthy control subjects. Video and sleep monitoring were performed on all twenty six participants for two consecutive nights. The first night evaluated the patient’s sleep duration, structure, and architecture of their dreams. During the second night of sleep evaluation, the researchers woke the subjects up as they entered the second non-REM sleep cycle, and again after 10 min of established REM sleep during the following sleep cycle, and asked them what they were dreaming before being woken up. The dream reports were then independently analysed and scored according to; complexity of dream, bizarreness, and elaboration.

Four of the thirteen patients with AAD reported dreaming when awakened from REM sleep, even though they demonstrated a mental blank during the daytime. This is compared to 12 out of 13 of the control patients. However, the four AAD patients’ dreams were devoid of any complex, bizarre, or emotional elements. The presence of simple yet spontaneous dreams in REM sleep, despite the absence of thoughts during wakefulness in AAD patients, supports the notion that simple dream imagery is generated by brainstem stimulation and sent to the sensory cortex. The lack of complexity in the dreams of the four AAD patients, as opposed to the complexity of the control patients’ dreams, demonstrates that the full dreaming process require these sensations to be interpreted by a higher-order cortical area.

Therefore, this study shows for the first time that it is the bottom-up process that causes the dream state.

Yet, despite the simplicity of the dreams, Isabelle Arnulf commented that the banal tasks that the AAD patients dreamt about were fascinating. For instance, Patient 10 dreamt of shaving – an activity he never initiated during the daytime without motivation from his caregivers, and an activity he could not do by himself due to severe hand dystonia. Similarly, Patient 5 dreamt about writing even though he would never write in the daytime without being invited by his caregivers to do so.

Interestingly, there were no real differences in the sleep measures between the AAD patients and the control patients apart from 46% of the AAD patients had a complete absence of sleep spindles (a burst of oscillatory brain activity visible on an EEG that occurs during stage 2 sleep). The striking absence of sleep spindles in localized lesions in the basal ganglia of these 6 AAD patients highlights the role of the pallidum and striatum in spindling activity during non-REM sleep. This is a key distinction between the AAD patients and the control patients; all thirteen control subjects displayed signs of sleep spindles.

(Source: alphagalileo.org)

Filed under auto-activation deficit brain activity REM sleep sensory cortex basal ganglia neuroscience science

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Discovery helps to unlock brain’s speech-learning mechanism

USC scientists have discovered a population of neurons in the brains of juvenile songbirds that are necessary for allowing the birds to recognize the vocal sounds they are learning to imitate.

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These neurons encode a memory of learned vocal sounds and form a crucial (and hitherto only theorized) part of the neural system that allows songbirds to hear, imitate and learn its species’ songs — just as human infants acquire speech sounds.

The discovery will allow scientists to uncover the exact neural mechanisms that allow songbirds to hear their own self-produced songs, compare them to the memory of the song that they are trying to imitate and then adjust their vocalizations accordingly.

Because this brain-behavior system is thought to be a model for how human infants learn to speak, understanding it could prove crucial to future understanding and treatment of language disorders in children. In both songbirds and humans, feedback of self-produced vocalizations is compared to memorized vocal sounds and progressively refined to achieve a correct imitation.

“Every neurodevelopmental disorder you can think of — including Tourette syndrome, autism and Rett syndrome — entails in some way a breakdown in auditory processing and vocal communication,” said Sarah Bottjer, senior author of an article on the research that appears in the Journal of Neuroscience on Sept. 4. “Understanding mechanisms of vocal learning at a cellular level is a huge step toward being able to someday address the biological issues behind the behavioral issues.”

Bottjer professor of neurobiology at the USC Dornsife College of Letters, Arts and Sciences, collaborated with lead author Jennifer Achiro, a graduate student at USC, to examine the activity of neurons in songbirds’ brains using electrodes to record the activity of individual neurons.

In the basal ganglia — a complex system of neurons in the brain responsible for, among other things, procedural learning — Bottjer and Achiro were able to isolate two different types of neurons in young songbirds: ones that were activated only when the birds heard themselves singing and others that were activated only when the birds heard the songs of adult birds that they were trying to imitate.

The two sets of neurons allow the songbirds to recognize both their current behavior and a goal behavior that they would like to achieve.

“The process of learning speech requires the brain to compare feedback of current vocal behavior to a memory of target vocal sounds,” Achiro said. “The discovery of these two distinct populations of neurons means that this brain region contains separate neural representation of current and goal behaviors. Now, for the first time, we can test how these two neural representations are compared so that correct matches between the two are somehow rewarded.”

The next step for scientists will be to learn how the brain rewards correct matches between feedback of current vocal behavior and the goal memory that depicts memorized vocal sounds as songbirds make progress in bringing their current behavior closer to their goal behavior, Bottjer said.

(Source: news.usc.edu)

Filed under songbirds neural activity basal ganglia vocal learning speech neuroscience science

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High-Resolution Mapping Technique Uncovers Underlying Circuit Architecture of the Brain

The power of the brain lies in its trillions of intercellular connections, called synapses, which together form complex neural “networks.” While neuroscientists have long sought to map these complex connections to see how they influence specific brain functions, traditional techniques have yet to provide the desired resolution. Now, by using an innovative brain-tracing technique, scientists at the Gladstone Institutes and the Salk Institute have found a way to untangle these networks. Their findings offer new insight into how specific brain regions connect to each other, while also revealing clues as to what may happen, neuron by neuron, when these connections are disrupted.

In the latest issue of Neuron, a team led by Gladstone Investigator Anatol Kreitzer, PhD, and Salk Investigator Edward Callaway, PhD, combined mouse models with a sophisticated tracing technique—known as the monosynaptic rabies virus system—to assemble brain-wide maps of neurons that connect with the basal ganglia, a region of the brain that is involved in movement and decision-making. Developing a better understanding of this region is important as it could inform research into disorders causing basal ganglia dysfunction, including Parkinson’s disease and Huntington’s disease.

“Taming and harnessing the rabies virus—as pioneered by Dr. Callaway—is ingenious in the exquisite precision that it offers compared with previous methods, which were messier with a much lower resolution,” explained Dr. Kreitzer, who is also an associate professor of neurology and physiology at the University of California, San Francisco, with which Gladstone is affiliated. “In this paper, we took the approach one step further by activating the tracer genetically, which ensures that it is only turned on in specific neurons in the basal ganglia. This is a huge leap forward technologically, as we can be sure that we’re following only the networks that connect to particular kinds of cells in the basal ganglia.”

At Gladstone, Dr. Kreitzer focuses his research on the role of the basal ganglia in Parkinson’s and other neurological disorders. Last year, he and his team published research that revealed clues to the relationship between two types of neurons found in the region—and how they guide both movement and decision-making. These two types, called direct-pathway medium spiny neurons (dMSNs) and indirect-pathway medium spiny neurons (iMSNs), act as opposing forces. dMSNs initiate movement, like the gas pedal, and iMSNs inhibit movement, like the brake. The latest research from the Kreitzer lab further found that these two types are also involved in behavior, specifically decision-making, and that a dysfunction of dMSNs or iMSNs is associated with addictive or depressive behaviors, respectively. These findings were important because they provided a link between the physical neuronal degeneration seen in movement disorders, such as Parkinson’s, and some of the disease’s behavioral aspects. But this study still left many questions unanswered.

“For example, while that study and others like it revealed the roles of dMSNs and iMSNs in movement and behavior, we knew very little about how other brain regions influenced the function of these two neuron types,” said Salk Institute Postdoctoral Fellow Nicholas Wall, PhD, the paper’s first author. “The monosynaptic rabies virus system helps us address that question.”

The system, originally developed in 2007 and refined by Wall and Callaway for targeting specific cell types in 2010, uses a modified version of the rabies virus to “infect” a brain region, which in turn targets neurons that are connected to it. When the system was applied in genetic mouse models, the team could see specifically how sensory, motor, and reward structures in the brain connected to MSNs in the basal ganglia. And what they found was surprising.

“We noticed that some regions showed a preference for transmitting to dMSNs versus iMSNs, and vice versa,” said Dr. Kreitzer. “For example, neurons residing in the brain’s motor cortex tended to favor iMSNs, while neurons in the sensory and limbic systems preferred dMSNs. This fine-scale organization, which would have been virtually impossible to observe using traditional techniques, allows us to predict the distinct roles of these two neuronal types.”

“These initial results should be treated as a resource not only for decoding how this network guides the vast array of very distinct brain functions, but also how dysfunctions in different parts of this network can lead to different neurological conditions,” said Dr. Callaway. “If we can use the rabies virus system to pinpoint distinct network disruptions in distinct types of disease, we could significantly improve our understanding of these diseases’ underlying molecular mechanisms—and get even closer to developing solutions for them.”

Filed under brain-tracing technique synapses neural networks brain mapping rabies virus basal ganglia neuroscience science

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'Strikingly similar' brains of man and fly may aid mental health research
A new study by scientists at King’s College London’s Institute of Psychiatry and the University of Arizona (UA) published in Science reveals the deep similarities in how the brain regulates behaviour in arthropods (such as flies and crabs) and vertebrates (such as fish, mice and humans).
The findings shed new light on the evolution of the brain and behaviour and may aid understanding of disease mechanisms underlying mental health problems.
Based on their own findings and available literature, Dr Frank Hirth (King’s) and Dr Nicholas Strausfeld (UA) compared the development and function of the central brain regions in arthropods (the ‘central complex’) and vertebrates (the ‘basal ganglia’).
Research suggests that both brain structures derive from embryonic stem cells at the base of the developing forebrain and that, despite the major differences between species, their respective constitutions and specifications derive from similar genetic programmes.
The authors describe that nerve cells in the central complex and the basal ganglia become inter-connected and communicate with each other in similar ways, facilitating the regulation of adaptive behaviours. In other words, the response of a fly or a mouse to internal stimuli such as hunger or sleep, and external stimuli such as light/dark or temperature, are regulated by similar neural mechanisms.
Dr Hirth from the Department of Neuroscience at King’s Institute of Psychiatry says: “Flies, crabs, mice, humans: all experience hunger, need sleep and have a preference for a comfortable temperature so we speculated there must be a similar mechanism regulating these behaviours. We were amazed to find just how deep the similarities go, despite the differences in size and appearance of these species and their brains.”
Dr Strausfeld, a Regents Professor in the UA’s Department of Neuroscience and the Director of the UA’s Center for Insect Science, says: “When you compare the two structures, you find that they are very similar in terms of how they’re organized. Their development is orchestrated by a whole suite of genes that are homologous between flies and mice, and the behavioral deficits resulting from disturbances in the two systems are remarkably similar as well.”
In humans, dysfunction of the basal ganglia can cause severe mental health problems ranging from autism, schizophrenia and psychosis, to neurodegeneration - as seen in Parkinson’s disease, motor neurone disease and dementia - as well as sleep disturbances, attention deficits and memory impairment. Similarly, when parts of the central complex are affected in fruit flies, they display similar impairments.
Dr Hirth (King’s) adds: “The deep similarities we see between how our brains and those of insects regulate behaviour suggest a common evolutionary origin. It means that prototype brain circuits, essential for behavioural choice, originated very early and have been maintained across animal species throughout evolutionary time. As surprising as it may seem, from insects’ dysfunctional brains, we can learn a great deal about how human brain disorders come about.”
The findings suggest that arthropod and vertebrate brain circuitries derive from a common ancestor already possessing a complex neural structure mediating the selection and maintenance of behavioural actions.
Although no fossil remains of the common ancestor exist, trace fossils, in the form of tracks criss-crossing the seafloor hundreds of millions of years ago, reveal purposeful changes in direction.
Dr Strausfeld (UA) says: “If you compare these tracks to the tracks left behind by a foraging fly larva on an agar plate or the tunnels made by a leaf-mining insect, they’re very similar. They all suggest that the animal chose to perform various different actions, and action selection is precisely what the central complex and the basal ganglia do.”
The trace fossils may thus support the early existence of brains complex enough to allow for action selection and a shared ancestry of neural structures between invertebrates and vertebrates.

'Strikingly similar' brains of man and fly may aid mental health research

A new study by scientists at King’s College London’s Institute of Psychiatry and the University of Arizona (UA) published in Science reveals the deep similarities in how the brain regulates behaviour in arthropods (such as flies and crabs) and vertebrates (such as fish, mice and humans).

The findings shed new light on the evolution of the brain and behaviour and may aid understanding of disease mechanisms underlying mental health problems.

Based on their own findings and available literature, Dr Frank Hirth (King’s) and Dr Nicholas Strausfeld (UA) compared the development and function of the central brain regions in arthropods (the ‘central complex’) and vertebrates (the ‘basal ganglia’).

Research suggests that both brain structures derive from embryonic stem cells at the base of the developing forebrain and that, despite the major differences between species, their respective constitutions and specifications derive from similar genetic programmes.

The authors describe that nerve cells in the central complex and the basal ganglia become inter-connected and communicate with each other in similar ways, facilitating the regulation of adaptive behaviours. In other words, the response of a fly or a mouse to internal stimuli such as hunger or sleep, and external stimuli such as light/dark or temperature, are regulated by similar neural mechanisms.

Dr Hirth from the Department of Neuroscience at King’s Institute of Psychiatry says: “Flies, crabs, mice, humans: all experience hunger, need sleep and have a preference for a comfortable temperature so we speculated there must be a similar mechanism regulating these behaviours. We were amazed to find just how deep the similarities go, despite the differences in size and appearance of these species and their brains.”

Dr Strausfeld, a Regents Professor in the UA’s Department of Neuroscience and the Director of the UA’s Center for Insect Science, says: “When you compare the two structures, you find that they are very similar in terms of how they’re organized. Their development is orchestrated by a whole suite of genes that are homologous between flies and mice, and the behavioral deficits resulting from disturbances in the two systems are remarkably similar as well.”

In humans, dysfunction of the basal ganglia can cause severe mental health problems ranging from autism, schizophrenia and psychosis, to neurodegeneration - as seen in Parkinson’s disease, motor neurone disease and dementia - as well as sleep disturbances, attention deficits and memory impairment. Similarly, when parts of the central complex are affected in fruit flies, they display similar impairments.

Dr Hirth (King’s) adds: “The deep similarities we see between how our brains and those of insects regulate behaviour suggest a common evolutionary origin. It means that prototype brain circuits, essential for behavioural choice, originated very early and have been maintained across animal species throughout evolutionary time. As surprising as it may seem, from insects’ dysfunctional brains, we can learn a great deal about how human brain disorders come about.”

The findings suggest that arthropod and vertebrate brain circuitries derive from a common ancestor already possessing a complex neural structure mediating the selection and maintenance of behavioural actions.

Although no fossil remains of the common ancestor exist, trace fossils, in the form of tracks criss-crossing the seafloor hundreds of millions of years ago, reveal purposeful changes in direction.

Dr Strausfeld (UA) says: “If you compare these tracks to the tracks left behind by a foraging fly larva on an agar plate or the tunnels made by a leaf-mining insect, they’re very similar. They all suggest that the animal chose to perform various different actions, and action selection is precisely what the central complex and the basal ganglia do.”

The trace fossils may thus support the early existence of brains complex enough to allow for action selection and a shared ancestry of neural structures between invertebrates and vertebrates.

Filed under fruit flies central complex basal ganglia nerve cells mental health evolution neuroscience science

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Intuition results from training
A game of Japanese chess reveals how experts develop their capacity for rapid problem-solving
The superior capability of experts to rapidly solve problems depends largely on their intuition, and it has long been known that this is related to experience and training. Although many psychological models relating to the development of intuition have been proposed to explain this phenomenon, none have been validated, and the underlying neural mechanisms remain a mystery.
Keiji Tanaka and colleagues from the Cognitive Brain Mapping Laboratory and Support Unit for Functional Magnetic Resonance Imaging at the RIKEN Brain Science Institute have now shown that activity in the basal ganglia of the brain, which is related to the automatic, rapid information processing or intuition characteristic of experts, develops during the course of training. The work provides a first insight into the neural response of the brain to extended training and hints at ways to improve the efficiency of training experts in industry.
In earlier work, another research team led by Tanaka showed that amateur players of the Japanese chess-like game of shogi plotted their best next-moves consciously using the human brain’s highly developed cerebral cortex. In contrast, they found that in professional players an important part of this process was unconscious or intuitive and had shifted to the head of the caudate nucleus in the basal ganglia, a much older part of the brain. This would leave the cortex free for higher-level strategy, the researchers suggested. Yet it remained unclear as to whether this shift of neural activity was entirely due to training, or dependent to some extent on pre-existing ability.
Tanaka’s most recent experiments involved training 20 novices for 15 weeks in mini-shogi, a simplified version of shogi. After about two weeks and again at the end of the 15-week program, the intuition of the volunteers was tested through their ability to come up with the best next-move to end-phase patterns of mini-shogi games. To ensure the answers were intuitive, each problem was presented for just two seconds and participants had to respond within three seconds. During this process, brain activity was recorded using functional magnetic resonance imaging (fMRI). The researchers found that activity in the caudate nucleus developed over the training period, whereas activity in the cortex remained unchanged.
“This work should open a fruitful interaction between the cognitive psychology of expertise development and biological studies of the basal ganglia,” says Tanaka. “We now would like to elucidate what computations the caudate nucleus conducts in generating the best next-move.”

Intuition results from training

A game of Japanese chess reveals how experts develop their capacity for rapid problem-solving

The superior capability of experts to rapidly solve problems depends largely on their intuition, and it has long been known that this is related to experience and training. Although many psychological models relating to the development of intuition have been proposed to explain this phenomenon, none have been validated, and the underlying neural mechanisms remain a mystery.

Keiji Tanaka and colleagues from the Cognitive Brain Mapping Laboratory and Support Unit for Functional Magnetic Resonance Imaging at the RIKEN Brain Science Institute have now shown that activity in the basal ganglia of the brain, which is related to the automatic, rapid information processing or intuition characteristic of experts, develops during the course of training. The work provides a first insight into the neural response of the brain to extended training and hints at ways to improve the efficiency of training experts in industry.

In earlier work, another research team led by Tanaka showed that amateur players of the Japanese chess-like game of shogi plotted their best next-moves consciously using the human brain’s highly developed cerebral cortex. In contrast, they found that in professional players an important part of this process was unconscious or intuitive and had shifted to the head of the caudate nucleus in the basal ganglia, a much older part of the brain. This would leave the cortex free for higher-level strategy, the researchers suggested. Yet it remained unclear as to whether this shift of neural activity was entirely due to training, or dependent to some extent on pre-existing ability.

Tanaka’s most recent experiments involved training 20 novices for 15 weeks in mini-shogi, a simplified version of shogi. After about two weeks and again at the end of the 15-week program, the intuition of the volunteers was tested through their ability to come up with the best next-move to end-phase patterns of mini-shogi games. To ensure the answers were intuitive, each problem was presented for just two seconds and participants had to respond within three seconds. During this process, brain activity was recorded using functional magnetic resonance imaging (fMRI). The researchers found that activity in the caudate nucleus developed over the training period, whereas activity in the cortex remained unchanged.

“This work should open a fruitful interaction between the cognitive psychology of expertise development and biological studies of the basal ganglia,” says Tanaka. “We now would like to elucidate what computations the caudate nucleus conducts in generating the best next-move.”

Filed under cerebral cortex basal ganglia problem-solving intuition neural activity neuroscience science

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When good habits go bad: Neuroscientist seeks roots of obsessive behavior, motion disorders

Learning, memory and habits are encoded in the strength of connections between neurons in the brain, the synapses. These connections aren’t meant to be fixed, they’re changeable, or plastic.

Duke University neurologist and neuroscientist Nicole Calakos studies what happens when those connections aren’t as adaptable as they should be in the basal ganglia, the brain’s “command center” for turning information into actions.

"The basal ganglia is the part of the brain that drives the car when you’re not thinking too hard about it," Calakos said. It’s also the part of the brain where neuroscientists are looking for the roots of obsessive-compulsive disorder, Huntington’s, Parkinson’s, and aspects of autism spectrum disorders.

In her most recent work, which she’ll discuss Saturday morning, Feb. 16 at the American Association for the Advancement of Science annual meeting in Boston, Calakos is mapping the defects in circuitry of the basal ganglia that underlie compulsive behavior. She is studying mice that have a synaptic defect that manifests itself as something like obsessive-compulsive behavior.

Calakos’ former colleague Guoping Feng developed the mice at Duke before moving to the McGovern Institute for Brain Research at MIT, where he now works. Feng was exploring the construction of synapses by knocking out genes one at a time. One set of mice ended up with facial lesions from endlessly grooming themselves until their faces were rubbed raw. When examining synaptic activity in the basal ganglia of these mice, Calakos’ group discovered that metabotropic glutamate receptors, or mGluRs, were overactive and this in turn, left their synapses less able to change. Scientists think overactivity of these receptors can cause many aspects of the autistic spectrum disorder Fragile X mental retardation.

"It’s an example of synaptic plasticity going awry," Calakos said. "They’re stuck with less adaptable synapses." Calakos is now using the mice to determine whether drugs that inhibit mGluRs can be used to improve their behavior and testing whether the circuit defects are a generalizable explanation for similar behaviors in other mouse models. This work may then lead to new understandings for compulsive behaviors and new treatment opportunities.

(Source: medicalxpress.com)

Filed under habits basal ganglia OCD compulsive behavior neuroscience science

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Exploring the Brain’s Relationship to Habits
The basal ganglia, structures deep in the forebrain already known to control voluntary movements, also may play a critical role in how people form habits, both bad and good, and in influencing mood and feelings.
"This system is not just a motor system," says Ann Graybiel. "We think it also strongly affects the emotional part of the brain."
Graybiel, an investigator at the McGovern Institute of the Massachusetts Institute of Technology and professor in MIT’s department of brain and cognitive sciences, believes that a core function of the basal ganglia is to help humans develop habits that eventually become automatic, including habits of thought and emotion.
"Many everyday movements become habitual through repetition, but we also develop habits of thought and emotion," she says."If cognitive and emotional habits are also controlled by the basal ganglia, this may explain why damage to these structures can lead not only to movement disorders, but also to repetitive and intrusive thoughts, emotions and desires."           
Graybiel’s research focuses on the brain’s relationship to habits—how we make or break them—and the neurobiology of the habit system. She and her team have identified and traced neural loops that run from the outer layer of the brain—“the thinking cap,” as she calls it—to a region called the striatum, which is part of the basal ganglia, and back again. These loops, in fact, connect sensory signals to habitual behaviors.
Her work ultimately could have an impact not just on such classic movement disorders as Parkinson’s and Huntington’s diseases, but in other conditions where repetitive movements commonly occur, such as Tourette Syndrome, autism, or obsessive-compulsive disorder, the latter when sufferers experience unwanted and repeated thoughts, feelings, ideas, sensations or behaviors that make them feel driven to do something, for example, repeatedly washing their hands.
Moreover, the research could have an immediate value for trying to understand “what happens in the brain as addiction occurs, as bad habits form, not just good habits,” she says. “There are many psychiatric and neurologic conditions in which these same brain regions are disordered.
"These conditions may in part be influenced by the very system we are working on," Graybiel adds. "We are working with models of anxiety and depression, stress and some of these movement disorders."
It turns out that the emotional circuits of the brain have strong ties to the striatum, she says. Graybiel’s research suggests that activity in the striatum strongly affects the emotional decisions that people make: whether to accept a good outcome or a potentially bad one, for example, and that there are circuits favoring good outcomes, and, surprisingly, other circuits that favor bad ones.
"This work ties into new research suggesting that there are brain systems for ‘good’ and brain systems for ‘bad,’" she says. "What is intriguing is that we may have identified the circuits that decide between the two."

Exploring the Brain’s Relationship to Habits

The basal ganglia, structures deep in the forebrain already known to control voluntary movements, also may play a critical role in how people form habits, both bad and good, and in influencing mood and feelings.

"This system is not just a motor system," says Ann Graybiel. "We think it also strongly affects the emotional part of the brain."

Graybiel, an investigator at the McGovern Institute of the Massachusetts Institute of Technology and professor in MIT’s department of brain and cognitive sciences, believes that a core function of the basal ganglia is to help humans develop habits that eventually become automatic, including habits of thought and emotion.

"Many everyday movements become habitual through repetition, but we also develop habits of thought and emotion," she says."If cognitive and emotional habits are also controlled by the basal ganglia, this may explain why damage to these structures can lead not only to movement disorders, but also to repetitive and intrusive thoughts, emotions and desires."           

Graybiel’s research focuses on the brain’s relationship to habits—how we make or break them—and the neurobiology of the habit system. She and her team have identified and traced neural loops that run from the outer layer of the brain—“the thinking cap,” as she calls it—to a region called the striatum, which is part of the basal ganglia, and back again. These loops, in fact, connect sensory signals to habitual behaviors.

Her work ultimately could have an impact not just on such classic movement disorders as Parkinson’s and Huntington’s diseases, but in other conditions where repetitive movements commonly occur, such as Tourette Syndrome, autism, or obsessive-compulsive disorder, the latter when sufferers experience unwanted and repeated thoughts, feelings, ideas, sensations or behaviors that make them feel driven to do something, for example, repeatedly washing their hands.

Moreover, the research could have an immediate value for trying to understand “what happens in the brain as addiction occurs, as bad habits form, not just good habits,” she says. “There are many psychiatric and neurologic conditions in which these same brain regions are disordered.

"These conditions may in part be influenced by the very system we are working on," Graybiel adds. "We are working with models of anxiety and depression, stress and some of these movement disorders."

It turns out that the emotional circuits of the brain have strong ties to the striatum, she says. Graybiel’s research suggests that activity in the striatum strongly affects the emotional decisions that people make: whether to accept a good outcome or a potentially bad one, for example, and that there are circuits favoring good outcomes, and, surprisingly, other circuits that favor bad ones.

"This work ties into new research suggesting that there are brain systems for ‘good’ and brain systems for ‘bad,’" she says. "What is intriguing is that we may have identified the circuits that decide between the two."

Filed under habitual behaviors habits sensory signals repetitive movements basal ganglia autism OCD striatum neuroscience science

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