Posts tagged brain

Posts tagged brain

The pilot and autopilot within our mind-brain connection
Have you ever driven to work so deep in thought that you arrive safely yet can’t recall the drive itself? And if so, what part of “you” was detecting cars and pedestrians, making appropriate stops and turns? Although when you get to work you can’t remember the driving experience, you are likely to have exquisite memory about having planned your day.
How does one understand this common experience? This is the question posed by Professor of Biology, John Lisman and his former undergraduate student, Eliezer J. Sternberg, now in medical school, in a recent paper in the Journal of Cognitive Neuroscience. Lisman explains that once a task such as driving has become a habit, you can perform another task at the same time, such as planning your day. But looking closer at these two behaviors, driving and planning, one can see interesting differences. The Habit system that is driving you to work is non-flexible: if the new parking regulations at work require you to go left instead or right, the likelihood that you’ll go right is very high. On the other hand, if you heard yesterday that your boss has scheduled a group meeting for noon, the likehood that you’ll plan your day accordingly is high. In other words, your non-habit system is flexible.
What interests Lisman and Sternberg is the relationship of the habit/non-habit systems to concepts of conscious vs unconscious. These concepts were popularized by Freud, who posited a duality of the human mind. Behavior can be influenced by both the conscious system and unconscious system. Freud compared the mind to an iceberg——with the small conscious system above water and the larger unconscious system below. Modern cognitive neuroscience now accepts this duality.
The mind can be described as having an unconscious and conscious part. And the brain can be described as having both habit and non-habit systems. Lisman and Sternberg argue that these two views can be merged: there is a habit system of which we are unconscious and a non-habit system of which we are conscious.
This simple equation turns out to have enormous implications for research on the mind-brain connection. Experiments on consciousness are done in humans because you can ask them to report their awareness, something you can’t do with animals. On the other hand, there are many invasive procedures for studying what’s happening in the brain of animals. So how can you study consciousness in rats?
Lisman and Sternberg provide a simple answer — ask whether rats have habit and non-habits. Scientific literature demonstrates that rats indeed have both habits and non-habits. For instance, when a rat comes to a choice point on a maze (and the reward site is to left), rats display very different behavior depending on how much experience they’ve had with that maze. With relatively little experience, rats pause at the choice point and look both ways before making a decision; in contrast, a highly experienced rats zooms left without stopping. Experiments have shown that different parts of the brain are involved in these two phases. Lisman and Sternberg make two conclusions: first, that rats, like us, have conscious and unconscious parts of the brain and second, that from experiments on rats we can learn to identify the parts of the brain that mediate conscious vs unconscious processes.
In their paper, Lisman and Sternberg also discuss potential objections to their hypothesis, and suggest further tests.
(Photo: GETTY)

Is There a Period of Increased Vulnerability for Repeat Traumatic Brain Injury?
Repeat traumatic brain injury affects a subgroup of the 3.5 million people who suffer head trauma each year. Even a mild repeat TBI that occurs when the brain is still recovering from an initial injury can result in poorer outcomes, especially in children and young adults. A metabolic marker that could serve as the basis for new mild TBI vulnerability guidelines is described in an article in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Journal of Neurotrauma website.
In an Editorial, “The Window of Risk in Repeated Head Injury,” accompanying this article, John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond, states that recent studies of TBI in animal models have shown that while repeat injury can exacerbate structural, functional, metabolic, and behavioral responses, “these responses only occur when the injury is repeated within a specific time frame post-injury.”
"Specifically, this window of risk is greatest when the interval between injuries is short, hours to days, while any risk for increased damage is obviated when the intervals between injuries are elongated over days to weeks," says Dr. Povlishock. It is not yet clear if these time periods of increased risk are age- or gender-specific or depend on the intensity of the initial injury.
A consistent finding following TBI in both humans and animal models is a decrease in glucose uptake by the brain. Mayumi Prins, Daya Alexander, Christopher Giza, and David Hovda, The UCLA Brain Injury Research Center, Los Angeles, CA, simulated single and repeat (after 1 or 5 days) mild TBI in rats and measured cerebral glucose metabolism. They tested the hypothesis that the rats’ brains would be more vulnerable to the damaging effects of repeat TBI at 1 day post-injury, when glucose metabolism was still decreased, than at 5 days, when it had returned to normal levels.
In the article, “Repeat Mild Traumatic Brain Injury: Mechanisms of Cerebral Vulnerability,” the authors propose that the duration of metabolic slowdown in the brain could serve as a valuable biomarker for how long a child might be at increased risk of repeat TBI.

Innovative system for the rehabilitation of people with brain damage
The Biomechanics Institute of Valencia (IBV) is currently taking part in the European project WALKX with the aim of developing an innovative rehabilitation system to improve the quality of life of people who have suffered brain damage. This system will allow home rehabilitation and improve patient’s autonomy.
WALKX is a two-year research project for the benefit of small and medium sized enterprises (SMEs), co-funded by the European Commission through the Seventh Framework Programme.
The user friendly walking training device the partners are designing will support the patient in raising from sitting to standing position and enable the patient to perform walking training and improve his/her manoeuvrability. “An upper body stabilizing and controllable supporting vest will be developed. Early in the rehabilitation process it will be used under supervision of a therapist, but with greatly reduced need for physical support from the therapists. This is intended to reduce the need for help from others and increase freedom of movement and personal autonomy of the patient”, said Ignacio Bermejo, Market Innovation Director at IBV.
One of the novelties of this device consists of a vest with attachment points on the patient’s waist in order to regulate the mobility of the trunk. Also, the device will be modular and low cost. The role of IBV in this initiative has been to define the design specifications and preclinical testing to validate the prototype. Preclinical tests are done in collaboration with the Department of Physical Medicine and Rehabilitation at the Hospital Universitari i Politècnic La Fe of Valencia.
The project is coordinated by the Norwegian company Made for Movement Group. Besides Biomechanics Institute, other members of the consortium are Innovatsiooni Eesti Instituut (Estonia), INNORA ROBOTICS (Greece), Newtrim and MCT (UK), ENIX (France), Motus (Italy) and MOBILE ROBOTICS SWEDEN (Sweden).
Stroke (cerebrovascular accident) is the most common cause of adult disability in Europe. Roughly 75% of victims survive, but about half of these lose the ability to live independently in their own home. As strokes often result in long term disability rather than death, the rehabilitation and hospitalisation represent a major economic burden for the EU of about €34 Bn annually. Currently, the annual incidence is approximately 2 per 1,000 inhabitants in the EU, and the number is predicted to double over the next 50 years due to the aging of the population.
As we age, it just may be the ability to filter and eliminate old information – rather than take in the new stuff – that makes it harder to learn, scientists report.
“When you are young, your brain is able to strengthen certain connections and weaken certain connections to make new memories,” said Dr. Joe Z. Tsien, neuroscientist at the Medical College of Georgia at Georgia Regents University and Co-Director of the GRU Brain & Behavior Discovery Institute.
It’s that critical weakening that appears hampered in the older brain, according to a study in the journal Scientific Reports.
The NMDA receptor in the brain’s hippocampus is like a switch for regulating learning and memory, working through subunits called NR2A and NR2B. NR2B is expressed in higher percentages in children, enabling neurons to talk a fraction of a second longer; make stronger bonds, called synapses; and optimize learning and memory. This formation of strong bonds is called long-term potentiation. The ratio shifts after puberty, so there is more NR2A and slightly reduced communication time between neurons.
When Tsien and his colleagues genetically modified mice that mimic the adult ratio – more NR2A, less NR2B – they were surprised to find the rodents were still good at making strong connections and short-term memories but had an impaired ability to weaken existing connections, called long-term depression, and to make new long-term memories as a result. It’s called information sculpting and adult ratios of NMDA receptor subunits don’t appear to be very good at it.
“If you only make synapses stronger and never get rid of the noise or less useful information then it’s a problem,” said Tsien, the study’s corresponding author. While each neuron averages 3,000 synapses, the relentless onslaught of information and experiences necessitates some selective whittling. Insufficient sculpting, at least in their mouse, meant a reduced ability to remember things short-term – like the ticket number at a fast-food restaurant – and long-term – like remembering a favorite menu item at that restaurant. Both are impacted in Alzheimer’s and age-related dementia.
All long-term depression was not lost in the mice, rather just response to the specific electrical stimulation levels that should induce weakening of the synapse. Tsien expected to find the opposite: that long-term potentiation was weak and so was the ability to learn and make new memories. “What is abnormal is the ability to weaken existing connectivity.”
Acknowledging the leap, this impaired ability could also help explain why adults can’t learn a new language without their old accent and why older people tend to be more stuck in their ways, the memory researcher said.
“We know we lose the ability to perfectly speak a foreign language if we learn than language after the onset of sexual maturity. I can learn English but my Chinese accent is very difficult to get rid of. The question is why,” Tsien said.
Tsien and his colleagues already have learned what happens when NR2B is overexpressed. He and East China Normal University researchers announced in 2009 the development of Hobbie-J, a smarter than average rat. A decade earlier, Tsien reported in the journal Nature the development of a smart mouse dubbed Doogie using the same techniques to over-express the NR2B gene in the hippocampus.
Doogie, Hobbie-J and their descendants have maintained superior memory as they age. Now Tsien is interested in following the NR2A over-expressing mouse to see what happens.
(Source: news.georgiahealth.edu)
Pannexins are abundant in the central nervous system of vertebrates
Pannexins traverse the cell membrane of vertebrate animals and form large pored channels. They are permeable for certain signalling molecules, such as the energy storage molecule ATP (adenosine triphosphate). The best known representative is Pannexin1, which occurs in abundance in the brain and spinal cord and among others in the hippocampus - a brain structure that is critical for long-term memory. Malfunctions of the pannexins play a role in the development of epilepsy and strokes.
No more scope in long-term potentiation
The research team studied mice in which the gene for Pannexin1 was lacking. Using cell recordings carried out on isolated brain sections, they analysed the long-term potentiation in the hippocampus. Long-term potentiation usually occurs when new memory content is built - the contacts between nerve cells are strengthened; they communicate more effectively with each other. In mice without Pannexin1, the long-term potentiation occurred earlier and was more prolonged than in mice with Pannexin1. “It looks at first glance like a gain in long-term memory”, says Nora Prochnow. “But precise analysis shows that there was no more scope for upward development.” Due to the lack of Pannexin1, the cell communication in general was increased to such an extent that a further increase through the learning of new knowledge was no longer possible. The synaptic plasticity was thus extremely restricted. “The plasticity is essential for learning processes in the brain”, Nora Prochnow explains. “It helps you to organise, keep or even to forget contents in a positive sense, to gain room for new inputs.”
Autistic-like behaviour without Pannexin1
The absence of Pannexin1 also had an impact on behaviour: when solving simple problems, the animals were quickly overwhelmed in terms of content. Their spatial orientation was limited, their attention impaired and an increased probability for seizure generation occurred. “The behavioural patterns are reminiscent of autism. We should therefore consider the Pannexin1 channel more closely with regard to the treatment of such diseases”, says the neurobiologist from Bochum.
Theory: feedback regulation gets out of hand without Pannexin1
According to the scientists’ theory, nerve cells lack a feedback mechanism without Pannexin1. Normally the channel protein releases ATP, which binds to specific receptors and thus reduces the release of the neurotransmitter glutamate. Without Pannexin1 more glutamate is released, which leads to increased long-term potentiation. This causes the cell to lose its dynamic equilibrium, which is needed for an efficient learning process.

It is said that classical music could make children more intelligent, but when you look at the scientific evidence, the picture is more mixed.
You have probably heard of the Mozart effect. It’s the idea that if children or even babies listen to music composed by Mozart they will become more intelligent. A quick internet search reveals plenty of products to assist you in the task. Whatever your age there are CDs and books to help you to harness the power of Mozart’s music, but when it comes to scientific evidence that it can make you more clever, the picture is more mixed.
The phrase “the Mozart effect” was coined in 1991, but it is a study described two years later in the journal Nature that sparked real media and public interest about the idea that listening to classical music somehow improves the brain. It is one of those ideas that feels plausible. Mozart was undoubtedly a genius himself, his music is complex and there is a hope that if we listen to enough of it, a little of that intelligence might rub off on us.
The idea took off, with thousands of parents playing Mozart to their children, and in 1998 Zell Miller, the Governor of the state of Georgia in the US, even asked for money to be set aside in the state budget so that every newborn baby could be sent a CD of classical music. It’s not just babies and children who were deliberately exposed to Mozart’s melodies. When Sergio Della Sala, the psychologist and author of the book Mind Myths, visited a mozzarella farm in Italy, the farmer proudly explained that the buffalos were played Mozart three times a day to help them to produce better milk.
I’ll leave the debate on the impact on milk yield to farmers, but what about the evidence that listening to Mozart makes people more intelligent? Exactly what was it was that the authors of the initial study discovered that took public imagination by storm?
When you look back at the original paper, the first surprise is that the authors from the University of California, Irvine are modest in their claims and don’t even use the “Mozart effect” phrase in the paper. The second surprise is that it wasn’t conducted on children at all: it was in fact conducted with those stalwarts of psychological studies – young adult students. Only 36 students took part. On three occasions they were given a series of mental tasks to complete, and before each task, they listened either to ten minutes of silence, ten minutes of a tape of relaxation instructions, or ten minutes of Mozart’s sonata for two pianos in D major (K448).
The students who listened to Mozart did better at tasks where they had to create shapes in their minds. For a short time the students were better at spatial tasks where they had to look at folded up pieces of paper with cuts in them and to predict how they would appear when unfolded. But unfortunately, as the authors make clear at the time, this effect lasts for about fifteen minutes. So it’s hardly going to bring you a lifetime of enhanced intelligence.
Brain arousal
Nevertheless, people began to theorise about why it was that Mozart’s music in particular could have this effect. Did the complexity of music cause patterns of cortical firing in the brain similar to those associated with solving spatial puzzles?
More research followed, and a meta-analysis of sixteen different studies confirmed that listening to music does lead to a temporary improvement in the ability to manipulate shapes mentally, but the benefits are short-lived and it doesn’t make us more intelligent.
Then it began to emerge that perhaps Mozart wasn’t so special after all. In 2010 a larger meta-analysis of a greater number of studies again found a positive effect, but that other kinds of music worked just as well. One study found that listening to Schubert was just as good, and so was hearing a passage read out aloud from a Stephen King novel. But only if you enjoyed it. So, perhaps enjoyment and engagement are key, rather than the exact notes you hear.
Although we tend to associate the Mozart effect with babies and small children, most of these studies were conducted on adults, whose brains are of course at a very different stage of development. But in 2006 a large study was conducted in Britain involving eight thousand children. They listened either to ten minutes of Mozart’s String Quintet in D Major, a discussion about the experiment or to a sequence of three pop songs: Blur’s “Country House,” “Return of the Mack,” by Mark Morrison and PJ and Duncan’s “Stepping Stone”. Once again music improved the ability to predict paper shapes, but this time it wasn’t a Mozart effect, but a Blur effect. The children who listened to Mozart did well, but with pop music they did even better, so prior preference could come into it.
Whatever your musical choice, it seems that all you need to do a bit better at predictive origami is some cognitive arousal. Your mind needs to get a little more active, it needs something to get it going and that’s going to be whichever kind of music appeals to you. In fact, it doesn’t have to be music. Anything that makes you more alert should work just as well – doing a few star jumps or drinking some coffee, for instance.
There is a way in which music can make a difference to your IQ, though. Unfortunately it requires a bit more effort than putting on a CD. Learning to play a musical instrument can have a beneficial effect on your brain. Jessica Grahn, a cognitive scientist at Western University in London, Ontario says that a year of piano lessons, combined with regular practice can increase IQ by as much as three points.
So listening to Mozart won’t do you or your children any harm and could be the start of a life-long love of classical music. But unless you and your family have some urgent imaginary origami to do, the chances are that sticking on a sonata is not going to make you better at anything.
(Source: bbc.com)

Out of Sight, Out of Mind? How the brain codes its surroundings beyond the field of view
Even when they are not directly in sight, we are aware of our surroundings: so it is that when our eyes are fixed on an interesting book, for example, we know that the door is to the right, the bookshelf is to the left and the window is behind us. However, research into the brain has so far concerned itself predominantly with how information from our field of vision is coded in the visual cortex. To date it has not been known how the brain codes our surroundings beyond the field of view from an egocentric perspective (that is, from the point of view of the observer).
In the latest issue of the renowned journal Current Biology, Andreas Schindler und Andreas Bartels, scientists at the Werner Reichardt Center for Integrative Neuroscience (CIN) of the University of Tübingen, present for the first time direct evidence of this kind of spatial information in the brain.
The participants in their study found themselves in the center of a virtual octagonal room, with a unique object in each corner. As the brain’s activity was monitored by means of functional magnetic resonance imaging, the participants stood in front of one corner and looked at its object. Now they were instructed to determine the position of a second randomly chosen object within the room relative to their current perspective (for example, the object behind them). After a few trials the participant turned around so that the next object was brought into the field of view and the task was set up again. The whole procedure was repeated until every object had been looked at once.
The scientists discovered that patterns of activity in the parietal cortex code the participant’s egocentric position, that is, the relative position to his or her surroundings. The spatial information discovered there proved to be independent of the particular object, its absolute position in the room or that of the observer – i.e. it encoded egocentric spatial information of the three-dimensional surroundings. This result turns out to be particularly interesting because damage to the brain in the parietal cortex can lead to serious disruption of egocentric spatial awareness. Hence it is difficult for patients suffering from optical ataxia to carry out coordinated grasping movements. Lesions in the parietal cortex can also lead to a symptom called spatial neglect where patients have difficulties in perceiving their surroundings on the side opposite to the lesion. The brain areas identified in the present study coincided precisely with the areas of brain damage in such patients and provide for the first time insights regarding their function in the healthy brain.
Cognitive deficits from concussions still present after two months
The ability to focus and switch tasks readily amid distractions was compromised for up to two months following brain concussions suffered by high school athletes, according to a study at the University of Oregon.
Research team members, in an interview, said the discovery suggests that some athletes may need longer recovery periods than current practices dictate to lower the risk of subsequent concussions. Conventional wisdom, said lead author David Howell, a graduate student in the UO Department of Human Physiology, says that typical recovery from concussion takes seven to 10 days.
"The differences we detected may be a matter of milliseconds between a concussed person and a control subject, but as far as brain time goes that difference for a linebacker returning to competition too soon could mean the difference between another injury or successfully preparing to safely tackle an oncoming running back," Howell said.
The findings are based on cognitive exercises used five times over the two months with a pair of sensitive computer-based measuring tools — the attentional network test and the task-switching test. The study focused on the effects of concussions to the frontal region of the brain, which is responsible for working, or short-term, memory and executive function, said Li-Shan Chou, professor of human physiology and director of the UO Motion Analysis Laboratory.
The study was published online ahead of print by Medicine & Science in Sports & Exercise, the official journal of the American College of Sports Medicine.
Can Blood Pressure Drugs Reduce the Risk of Dementia?
People taking the blood pressure drugs called beta blockers may be less likely to have changes in the brain that can be signs of Alzheimer’s disease and other types of dementia, according to a study released today that will be presented at the American Academy of Neurology’s 65th Annual Meeting in San Diego, March 16 to 23, 2013. The study involved 774 elderly Japanese-American men who took part in the Honolulu-Asia Aging Study. Autopsies were performed on the men after their death. Of the 774 men, 610 had high blood pressure or were being treated with medication for high blood pressure. Among those who had been treated (about 350), 15 percent received only a beta blocker medication, 18 percent received a beta blocker plus one or more other medications, and the rest of the participants received other blood pressure drugs.
The study found that all types of blood pressure treatments were clearly better than no treatment. However, men who had received beta blockers as their only blood pressure medication had fewer abnormalities in their brains compared to those who had not been treated for their hypertension, or who had received other blood pressure medications. The brains of participants who had received beta blockers plus other medications showed an intermediate reduction in numbers of brain abnormalities.
These included two distinct types of brain lesion: those indicating Alzheimer’s disease, and lesions called microinfarcts, usually attributed to tiny, multiple, unrecognized strokes. Study participants who had taken beta blockers alone or in combination with another blood pressure medication had significantly less shrinkage in their brains.
“With the number of people with Alzheimer’s disease expected to grow significantly as our population ages, it is increasingly important to identify factors that could delay or prevent the disease,” said study author Lon White, MD, of the Pacific Health Research and Education Institute in Honolulu. “These results are exciting, especially since beta blockers are a common treatment for high blood pressure.”
Earlier research has shown that high blood pressure in midlife is a strong risk factor for dementia.
Botox may help stroke patients
Injecting botox into the arm muscles of stroke survivors, with severe spasticity, changes electrical activity in the brain and may assist with longer-term recovery, according to new research.
Researchers at NeuRA (Neuroscience Research Australia) monitored nerve activity in the arms and brains of stroke survivors before and after botulinum toxin (botox) injections in rigid and stiff muscles in the arm.
They found that botox indeed improved arm muscles, but also altered brain activity in the cortex – the brain region responsible for movement, memory, learning and thinking.
“Botulinum toxin is used to treat a range of muscular and neurological conditions and our data shows that this treatment results in electrical and functional changes within the brain itself”, says Dr William Huynh, lead author of the study and a research neurologist at NeuRA.
“This effect of botox on the brain may arise because the toxin travels to the central nervous system directly, or because muscles treated with botox are sending different signals back to the brain”.
“Either way, we found that botox treatment in affected muscles not only improves muscle disorders in stroke patients, but also normalises electrical activity in the brain, particularly in the half of the brain not damaged by stroke”.
“Restoring normal activity in the unaffected side of the brain is particularly important because we suspect that abnormal information sent from affected muscles to the brain may be disrupting patients’ long-term recovery”, Dr Huynh concluded.
This paper is published in the journal Muscle and Nerve.