The area of the brain responsible for self-control is separate from the area associated with taking action.
Image Above: Brain area in the fronto-median cortex that was activated when participants intentionally withhold a planned action in the last moment
The results illuminate a very important aspect of the brain's control of behavior, the ability to hold off doing something after you've developed the intention to do it-one might call it 'free won't' as opposed to free will," says Martha Farah, PhD, of the University of Pennsylvania. "It is very important to identify the circuits that enable 'free won't' because of the many psychiatric disorders for which self-control problems figure prominently-from attention deficit disorder to substance dependence and various personality disorders." Farah was not involved in the experiment.
The findings broaden understanding of the neural basis for decision making, or free will, and may help explain why some individuals are impulsive while others are reluctant to act, says lead author Marcel Brass, PhD, of the Max Planck Institute for Human Cognitive and Brain Sciences and Ghent University. Brass and Patrick Haggard, PhD, of University College London, used functional magnetic resonance imaging (fMRI) to study the brain activity of participants pressing a button at times they chose themselves. They compared data from these trials to results when the participants prepared to hit the button, then decided to hold back or veto the action.
Fifteen right-handed participants were asked to press a button on a keyboard. They were asked to choose some cases in which they stopped just before pressing the button. Participants also indicated on a clock the time at which they intended to press the button or decided to hold back. When Brass and Haggard compared fMRI images of the two scenarios, they found that pulling back yielded activity in the dorsal fronto-median cortex (dFMC), an area on the midline of the brain directly above the eyes, which did not show up when participants followed through and made the action. In addition, those who chose to stop the intended action most often showed greatest contrast in dFMC activity.
"The capacity to withhold an action that we have prepared but reconsidered is an important distinction between intelligent and impulsive behavior," says Brass, "and also between humans and other animals."
Future study will involve methods with a better time resolution such as EEG to determine whether the inhibitory process could operate in the brief time period between the time of conscious intention and the point of no return for motor output.
Image: Max Planck Institute for Human Cognitive and Brain Sciences
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Milestone In The Regeneration Of Brain Cells
Brain Cells Work Differently Than Previously Thought
One Step Closer To Transplanting Stem Cells In The Brain
Researchers Identify Brain Network That May Help Prevent Or Slow Alzheimer's
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Friday, 24 August 2007
Tuesday, 21 August 2007
Ancestors help Bird Memory
Birds learn to fly with a little help from their Ancestors
A University of Sheffield researcher has discovered that the reason birds learn to fly so easily is because latent memories may have been left behind by their ancestors.
It is widely known that birds learn to fly through practice, gradually refining their innate ability into a finely tuned skill, and these skills may be easy to refine because of a genetically specified latent memory for flying.
Dr Dr Jim Stone from the University of Sheffield´s Department of Psychology, used simple models of brains called artificial neural networks and computer simulations to test his theory.
He discovered that learning in previous generations indirectly induces the formation of a latent memory in the current generation and therefore decreases the amount of learning required. These effects are especially pronounced if there is a large biological 'fitness cost' to learning, where biological fitness is measured in terms of the number of offspring each individual has.
The beneficial effects of learning also depend on the unusual form of information storage in neural networks. Unlike computers, which store each item of information in a specific location in the computer's memory chip, neural networks store each item distributed over many neuronal connections. If information is stored in this way then evolution is accelerated, explaining how complex motor skills, such as nest building and hunting skills, are acquired by a combination of innate ability and learning over many generations.
However not every bird automatically knows how to fly.
A crowling which has been blown from its nest, had a great fall and hurt its legs, may never fly - though there be nothing wrong with its wings at all. Birds learn fear, pain and doubt too. - Q9
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New Caledonian Crows Find Two Tools Better Than One
Uncertainties Of Savanna Habitat Drive Birds To Cooperative Breeding
Birds With Child-care Assistance Invest Less In Eggs @ Science Daily
Are Artist's Born or Taught from Hank @ Scientific Blogging
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Friday, 10 August 2007
Functioning Neuron Produced
Scientists with the Institute of Stem Cell Biology and Medicine at UCLA were able to produce from human embryonic stem cells a highly pure, large quantity of functioning neurons that will allow them to create models of and study diseases such as Alzheimer's, Parkinson's, prefrontal dementia and schizophrenia.
Researchers previously had been able to produce neurons - the impulse-conducting cells in the brain and spinal cord - from human embryonic stem cells. However, the percentage of neurons in the cell culture was not high and the neurons were difficult to isolate from the other cells.
UCLA's Yi Sun, an associate professor of biobehavioural sciences, and Howard Hughes Medical Institute investigator Thomas Südhof at the University of Texas Southwestern Medical Center were able to produce 70 to 80 percent of neurons in cell culture. Sun and Südhof also were able to isolate the neurons and determine that they had a functional synaptic network, which the neurons use to communicate. Because they were functional, the neurons can be used to create a variety of human neurological disease models.
"Previously, the system to grow and isolate neurons was very messy and it was unknown whether those neurons were functioning," Sun said. "We're excited because we have been able to purify so many more neurons out of the cell culture and they were, surprisingly, healthy enough to form synapses. These cells will be excellent for doing gene expression studies and biochemical and protein analyses."
Sun's method prodded human embryonic stem cells to differentiate into neural stem cells, the cells that give rise to neurons. When the time was right, Sun's team added protein growth factors into the cell culture that stopped the neural stem cells from self-renewing and prodded them into differentiating into neurons.
To isolate the cells, Sun and her team added an enzyme that digests a sort of protein matrix that holds cells in culture together. The neurons could then be separated from the neural stem cells that had not yet differentiated, a sort of chemical round-up that isolated the neurons. The cells were then put into a cell strainer that allowed passage through of the isolated neurons.
The large number of pure neurons produced will allow Sun and her team to study their biological form and structure, the genes they express, the development of synapses and the electric and chemical communication activities within the synapse network.
"We will be able to study the cellular properties of neurons in a very defined way that will maybe tell us what goes wrong in diseases such as Alzheimer's and Parkinson's," Sun said. "We're currently creating many models of human neurological diseases that may provide the answers we're looking for. We don't know what causes prefrontal dementia, Huntington's disease or schizophrenia. The key is likely in the quality of neuronal communications. By studying the chemical and electrical transmissions, we may be able to determine what goes wrong that leads to these debilitating diseases and find a way to stop or treat it."
Sun will be among the first researchers to be able to study true neuron function.
A second important discovery in Sun's study showed that two embryonic stem cells lines derived in similar manners, and therefore expected to behave similarly when differentiating, did not. Using the same techniques to prod the two embryonic stem cells lines to differentiate, Sun found that one line had a bias to become neurons that are found in the forebrain. The other line differentiated into neurons found in rear portions of the brain and spinal cord. The finding was surprising, and significant, Sun said.
"The realization that not all human embryonic stem cell lines are born equal is critical," Sun said. "If you're studying a disease found in a certain part of the brain, you should use a human embryonic stem cell line that produces the neurons from that region of the brain to get the most accurate results from your study.
Huntington's disease, for example, is a forebrain disease, so the neurons should be differentiated from a cell line that is biased to produce neurons from the forebrain."Sun said there are ways to prod an embryonic stem cell line biased to become neurons found in the rear brain to become neurons found in the forebrain. However, there are limits to how much prodding can be done.
Sun and her team confirmed that the two embryonic stem cell lines were different through gene expression analysis - neurons that perform different functions in different parts of the brain express different genes.
The cell line prone to becoming neurons found in the forebrain expressed genes typically found in those neurons, while the other line expressed genes found in the rear brain and spinal cord.
The team now are studying why the two human embryonic stem cell lines have biases to become different types of neurons. "If we knew that, we might be able to tweak or alter whatever is driving the bias so that limitation in the stem cell line could be bypassed," Sun said.
Study results were recently published in an early online edition of the journal Proceedings of the National Academy of Sciences.
Functioning Neurons From Human Embryonic Stem Cells Produced
UCLA Institute of Stem Cell Biology
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Wednesday, 8 August 2007
Pain Perception
Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently transmitted and perpetuated.
Clinical pain is a serious public health issue.
Our understanding of the neural correlates of pain perception in humans has improved with the advent of neuroimaging. Relating neural activity changes to the varied pain experiences has led to an increased awareness of how factors (e.g., cognition, emotion, context, injury) can separately influence pain perception.
It has been suggested that the brainstem plays a pivotal role in gating the degree of nociceptive transmission so that the resultant pain experienced is appropriate for the particular situation of the individual.
Pain that persists for more than three months is defined as chronic and as such is one of largest medical health problems in the developed world. While the management and treatment of acute pain is reasonably good, the needs of chronic pain sufferers are largely unmet, creating an enormous emotional and financial burden to sufferers, carers, and society.
The mechanisms that contribute to the generation and maintenance of a chronic pain state are increasingly investigated and better understood. A consequent shift in mindset that treats chronic pain as a disease rather than a symptom is accelerating advances in this field considerably.
Pain is a conscious experience, an interpretation of the nociceptive input influenced by memories, emotional, pathological, genetic, and cognitive factors. Resultant pain is not necessarily related linearly to the nociceptive drive or input; neither is it solely for vital protective functions. This is especially true in the chronic pain state. Furthermore, the behavioral response by a subject to a painful event is modified according to what is appropriate or possible in any particular situation. Pain is, therefore, a highly subjective experience “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”
By its very nature, pain is therefore difficult to assess, investigate, manage, and treat. Figure 1 (above) illustrates the mixture of factors that we know influence nociceptive inputs to amplify, attenuate, and color the pain experience.
Because pain is a complex, multifactorial subjective experience, a large distributed brain network is subsequently accessed during nociceptive processingm and was first described this as the pain “neuromatrix,” but it's now more commonly referred to as the “pain matrix”; simplistically it can be thought of as having lateral (sensory-discriminatory) and medial (affective-cognitive-evaluative) neuroanatomical components. However, because different brain regions play a more or less active role depending upon the precise interplay of the factors involved in influencing pain perception (e.g., cognition, mood, injury, and so forth), what comprises the pain matrix is not unequivocally defined.
For both chronic and acute pain sufferers, mood and emotional state has a significant impact on the resultant pain perception and ability to cope. For example, it is a common clinical and experimental observation that anticipating and being anxious about pain can exacerbate the pain experienced. Anticipating pain is highly adaptive; we all learn in early life to avoid hot pans on stoves and not to put your finger into a candle flame. However, for the chronic pain patient it becomes maladaptive and can lead to fear of movement, avoidance, anxiety, and so forth.
Another negative cognitive and mood affect that impacts pain is catastrophizing. This construct incorporates magnification of pain-related symptoms, rumination about pain, feelings of helplessness, and pessimism about pain-related outcomes, and it is defined as a set of negative emotional and cognitive processes. A study on fibromyalgia patients found that pain catastrophizing, independent of the influence of depression, was significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala), and motor control.
Clearly, these results support the notion that catastrophizing influences pain perception through altering attention and anticipation, as well as heightening emotional responses to pain.
It is interesting to speculate whether activity in such “emotional” brain regions due to chronic pain impacts performance in tasks requiring emotional decision making. A card game developed to study emotional decision making, chronic pain patients displayed a specific cognitive deficit compared to controls, suggesting such an impact might exist in everyday life.
Such experiments are hard to reproduce in animal studies.
As the problem of pain and the key role of the brain becomes increasingly well recognized, more research is being directed toward a better understanding of the underlying mechanisms. Some of the newest and more novel areas of investigation are briefly summarized here.
The recent finding that significant atrophy exists in the brains of chronic pain patients highlights the need to perform more advanced structural imaging measures and image analyses to quantify fully these effects.
Determining what the possible causal factors are that produce such neurodegeneration is difficult. Candidates include the chronic pain condition itself (i.e., excitotoxic events due to barrage of nociceptive inputs), the pharmacological agents prescribed, or perhaps the physical lifestyle change subsequent to becoming a chronic pain patient.
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Backache Sufferers Who Fear Pain Change Movements from Science Daily
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Clinical pain is a serious public health issue.
Our understanding of the neural correlates of pain perception in humans has improved with the advent of neuroimaging. Relating neural activity changes to the varied pain experiences has led to an increased awareness of how factors (e.g., cognition, emotion, context, injury) can separately influence pain perception.
It has been suggested that the brainstem plays a pivotal role in gating the degree of nociceptive transmission so that the resultant pain experienced is appropriate for the particular situation of the individual.
Pain that persists for more than three months is defined as chronic and as such is one of largest medical health problems in the developed world. While the management and treatment of acute pain is reasonably good, the needs of chronic pain sufferers are largely unmet, creating an enormous emotional and financial burden to sufferers, carers, and society.
The mechanisms that contribute to the generation and maintenance of a chronic pain state are increasingly investigated and better understood. A consequent shift in mindset that treats chronic pain as a disease rather than a symptom is accelerating advances in this field considerably.
Pain is a conscious experience, an interpretation of the nociceptive input influenced by memories, emotional, pathological, genetic, and cognitive factors. Resultant pain is not necessarily related linearly to the nociceptive drive or input; neither is it solely for vital protective functions. This is especially true in the chronic pain state. Furthermore, the behavioral response by a subject to a painful event is modified according to what is appropriate or possible in any particular situation. Pain is, therefore, a highly subjective experience “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”
By its very nature, pain is therefore difficult to assess, investigate, manage, and treat. Figure 1 (above) illustrates the mixture of factors that we know influence nociceptive inputs to amplify, attenuate, and color the pain experience.
Because pain is a complex, multifactorial subjective experience, a large distributed brain network is subsequently accessed during nociceptive processingm and was first described this as the pain “neuromatrix,” but it's now more commonly referred to as the “pain matrix”; simplistically it can be thought of as having lateral (sensory-discriminatory) and medial (affective-cognitive-evaluative) neuroanatomical components. However, because different brain regions play a more or less active role depending upon the precise interplay of the factors involved in influencing pain perception (e.g., cognition, mood, injury, and so forth), what comprises the pain matrix is not unequivocally defined.
For both chronic and acute pain sufferers, mood and emotional state has a significant impact on the resultant pain perception and ability to cope. For example, it is a common clinical and experimental observation that anticipating and being anxious about pain can exacerbate the pain experienced. Anticipating pain is highly adaptive; we all learn in early life to avoid hot pans on stoves and not to put your finger into a candle flame. However, for the chronic pain patient it becomes maladaptive and can lead to fear of movement, avoidance, anxiety, and so forth.
Another negative cognitive and mood affect that impacts pain is catastrophizing. This construct incorporates magnification of pain-related symptoms, rumination about pain, feelings of helplessness, and pessimism about pain-related outcomes, and it is defined as a set of negative emotional and cognitive processes. A study on fibromyalgia patients found that pain catastrophizing, independent of the influence of depression, was significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala), and motor control.
Clearly, these results support the notion that catastrophizing influences pain perception through altering attention and anticipation, as well as heightening emotional responses to pain.
It is interesting to speculate whether activity in such “emotional” brain regions due to chronic pain impacts performance in tasks requiring emotional decision making. A card game developed to study emotional decision making, chronic pain patients displayed a specific cognitive deficit compared to controls, suggesting such an impact might exist in everyday life.
Such experiments are hard to reproduce in animal studies.
As the problem of pain and the key role of the brain becomes increasingly well recognized, more research is being directed toward a better understanding of the underlying mechanisms. Some of the newest and more novel areas of investigation are briefly summarized here.
The recent finding that significant atrophy exists in the brains of chronic pain patients highlights the need to perform more advanced structural imaging measures and image analyses to quantify fully these effects.
Determining what the possible causal factors are that produce such neurodegeneration is difficult. Candidates include the chronic pain condition itself (i.e., excitotoxic events due to barrage of nociceptive inputs), the pharmacological agents prescribed, or perhaps the physical lifestyle change subsequent to becoming a chronic pain patient.
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Backache Sufferers Who Fear Pain Change Movements from Science Daily
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Monday, 6 August 2007
Music on the Brain
Music moves brain to pay attention
Using brain images of people listening to short symphonies by an obscure 18th-century composer, a research team from the Stanford University School of Medicine has gained valuable insight into how the brain sorts out the chaotic world around it.
The research team showed that music engages the areas of the brain involved with paying attention, making predictions and updating the event in memory. Peak brain activity occurred during a short period of silence between musical movements—when seemingly nothing was happening.
Beyond understanding the process of listening to music, their work has far-reaching implications for how human brains sort out events in general. The findings are published in the Aug. 2 issue of Neuron.
The researchers caught glimpses of the brain in action using functional magnetic resonance imaging, or fMRI, which gives a dynamic image showing which parts of the brain are working during a given activity. The goal of the study was to look at how the brain sorts out events, but the research also revealed that musical techniques used by composers 200 years ago help the brain organize incoming information.
The team used music to help study the brain’s attempt to make sense of the continual flow of information the real world generates, a process called event segmentation. The brain partitions information into meaningful chunks by extracting information about beginnings, endings and the boundaries between events.
See Video & Read more @ Stanford University School Of Medicine news release
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Nerve Cell Modulator Could Help With Mood Disorders
Virtual Navigation - Rethinking How Columbus Mentally Found His Way
Connectivity Between Brain Areas Leads To Human Knowledge
Prefrontal Cortex Differences Mean Richer Memories For Adults
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Thursday, 2 August 2007
Neuro Genesis in Korea?
Toward An Alternative To Stem Cells For Treating Chronic Brain Diseases
Image Courtesy of Injae Shin, Yonsei University, Korea.
Scientists in Korea are reporting the first successful use of a drug-like molecule to transform human muscle cells into nerve cells. This advance could lead to new treatments for stroke, Alzheimer's disease, Parkinson's disease and other neurological disorders.
The researchers exposed immature mouse muscle cells myoblasts (image left) growing in laboratory cell cultures to neurodazine, a synthetic small molecule. After one week, 40-50 percent of the myoblasts were transformed into cells that resembled both the structure and function of nerve cells (image right), including expression of neuron-specific proteins. Additional studies showed a similar transformation in a group of human skeletal muscle cells that were exposed to the same chemical for several days, they add.
"In conclusion, we have developed the first small molecule that can induce neurogenesis of non-pluripotent myoblasts and the cells derived from mature, human skeletal muscle," the report states. "These studies build upon recent research illustrating the value of chemical approaches for providing tools that differentiate lineage-committed cells into other cell types."
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MS breakthrough new genetic risk factors discovered
Rare Example of Darwinism Seen in Action - UC Riverside release
Factor That Causes Embryonic Stem Cell Specialization from Scientific Blogging
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Image Courtesy of Injae Shin, Yonsei University, Korea.
Scientists in Korea are reporting the first successful use of a drug-like molecule to transform human muscle cells into nerve cells. This advance could lead to new treatments for stroke, Alzheimer's disease, Parkinson's disease and other neurological disorders.
The researchers exposed immature mouse muscle cells myoblasts (image left) growing in laboratory cell cultures to neurodazine, a synthetic small molecule. After one week, 40-50 percent of the myoblasts were transformed into cells that resembled both the structure and function of nerve cells (image right), including expression of neuron-specific proteins. Additional studies showed a similar transformation in a group of human skeletal muscle cells that were exposed to the same chemical for several days, they add.
"In conclusion, we have developed the first small molecule that can induce neurogenesis of non-pluripotent myoblasts and the cells derived from mature, human skeletal muscle," the report states. "These studies build upon recent research illustrating the value of chemical approaches for providing tools that differentiate lineage-committed cells into other cell types."
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MS breakthrough new genetic risk factors discovered
Rare Example of Darwinism Seen in Action - UC Riverside release
Factor That Causes Embryonic Stem Cell Specialization from Scientific Blogging
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