Posts tagged science

ScienceDaily (Feb. 3, 2012) — When a friend tells you she had a rough day, do you feel sandpaper under your fingers? The brain may be replaying sensory experiences to help understand common metaphors, new research suggests.

Regions of the brain activated by hearing textural metaphors are shown in green. Yellow and red show regions activated by sensory experience of textures visually and through touch. (Credit: Image courtesy of Emory University)

Linguists and psychologists have debated how much the parts of the brain that mediate direct sensory experience are involved in understanding metaphors. George Lakoff and Mark Johnson, in their landmark work ‘Metaphors we live by’, pointed out that our daily language is full of metaphors, some of which are so familiar (like “rough day”) that they may not seem especially novel or striking. They argued that metaphor comprehension is grounded in our sensory and motor experiences.

New brain imaging research reveals that a region of the brain important for sensing texture through touch, the parietal operculum, is also activated when someone listens to a sentence with a textural metaphor. The same region is not activated when a similar sentence expressing the meaning of the metaphor is heard.

The results were published online this week in the journal Brain & Language.

"We see that metaphors are engaging the areas of the cerebral cortex involved in sensory responses even though the metaphors are quite familiar," says senior author Krish Sathian, MD, PhD, professor of neurology, rehabilitation medicine, and psychology at Emory University. "This result illustrates how we draw upon sensory experiences to achieve understanding of metaphorical language."

Sathian is also medical director of the Center for Systems Imaging at Emory University School of Medicine and director of the Rehabilitation R&D Center of Excellence at the Atlanta Veterans Affairs Medical Center.

Seven college students who volunteered for the study were asked to listen to sentences containing textural metaphors as well as sentences that were matched for meaning and structure, and to press a button as soon as they understood each sentence. Blood flow in their brains was monitored by functional magnetic resonance imaging. On average, response to a sentence containing a metaphor took slightly longer (0.84 vs 0.63 seconds).

In a previous study, the researchers had already mapped out, for each of these individuals, which parts of the students’ brains were involved in processing actual textures by touch and sight. This allowed them to establish with confidence the link within the brain between metaphors involving texture and the sensory experience of texture itself.

"Interestingly, visual cortical regions were not activated by textural metaphors, which fits with other evidence for the primacy of touch in texture perception," says research associate Simon Lacey, PhD, the first author of the paper.

The researchers did not find metaphor-specific differences in cortical regions well known to be involved in generating and processing language, such as Broca’s or Wernicke’s areas. However, this result doesn’t rule out a role for these regions in processing metaphors, Sathian says. Also, other neurologists have seen that injury to various areas of the brain can interfere with patients’ understanding of metaphors.

"I don’t think that there’s only one area responsible for metaphor processing," Sathian says. "Actually, several recent lines of research indicate that engagement with abstract concepts is distributed around the brain." "I think our research highlights the role of neural networks, rather than a single area of the brain, in these processes. What could be happening is that the brain is conducting an internal simulation as a way to understand the metaphor, and that’s why the regions associated with touch get involved. This also demonstrates how complex processes involving symbols, such as appreciating a painting or understanding a metaphor, do not depend just on evolutionarily new parts of the brain, but also on adaptations of older parts of the brain."

Sathian’s future plans include asking whether similar relationships exist for other senses, such as vision. The researchers also plan to probe whether magnetic stimulation of the brain in regions associated with sensory experience can interfere with understanding metaphors.

The research was supported by the National Institutes of Health and the National Science Foundation.

Source: ScienceDaily

Article Date: 04 Feb 2012 - 10:00 PST

The February edition of Neurosurgery reports that animal experiments in brain-injured rats have shown that stem cells injected via the carotid artery travel directly to the brain, greatly enhancing functional recovery. The study demonstrates, according to leading researcher Dr Toshiya Osanai, of Hokkaido University Graduate School of Medicine in Sapporo, Japan, that the carotid artery injection technique could, together with some form of in-vivo optical imaging to track the stem cells after transplantation, potentially be part of a new approach for stem cell transplantation in human brain trauma injuries (TBI).

Dr. Osanai and team assessed a new “intra-arterial” technique of stem cell transplantation in rats, with the aim of delivering the stem cells directly to the brain without having to go through the general circulation. They induced TBI in the animals before injecting stem cells into the carotid artery seven days later.

The stem cells were obtained from the rats’ bone marrow and were labeled with “quantum dots” prior to being injected. Quantom dots are a biocompatible, fluorescent semiconductor created with nanotechnology that emit near-infrared light with much longer wavelengths that penetrate bone and skin, enabling a non-invasive method of monitoring the stem cells for a period of four weeks following transplantation.

This in vivo optical imaging technique enabled the scientists to observe that the injected stem cells entered the brain on the first attempt, without entering the general circulation. They observed that the stem cells started migrating from the capillaries into the injured part of the brain within three hours.

At week 4, the researchers noted that the rats in the stem cell transplant group achieved a substantial recovery of motor function, compared with the untreated animals that had no signs of recovery.

The team learnt, after examining the treated brains, that the stem cells had transformed into different brain cell types and aided in healing the injured brain area.

Over the last few years, the potential of stem cell therapy for curing and treating illnesses and conditions has been growing rapidly. Below is a list of some of its possible uses.

(Photo by: Mikael Häggström)

Developing stem cell therapy for brain injury in human patients

Stem cells represent a potential, new important method of treatment for those who suffered brain injuries, TBI and stroke. But even though bone marrow stem cells, similar to the ones used in the new study, are a promising source of donor cells, many questions remain open regarding the optimal timing, dose and route of stem cell delivery.

In the new animal study, the rats were injected with the stem cells one week after TBI. This is a “clinically relevant” time, given that this is the minimum time it takes to develop stem cells from bone marrow.

Transplanting the stem cells into the carotid artery is a fairly simple procedure that delivers the cells directly to the brain.

The experiments have also provided key evidence that stem cell treatment can promote healing after TBI with a substantial recovery of function.

Dr. Osanai and team write that by using in vivo optical imaging:

"The present study was the first to successfully track donor cells that were intra-arterially transplanted into the brain of living animals over four weeks."

A similar form of imaging technology could also prove beneficial for monitoring the effects of stem cell transplantation in humans, although the tracking will pose challenges, due to the human skull and scalp being much thicker than in rats.

The researchers conclude:

"Further studies are warranted to apply in vivo optical imaging clinically.”

Written by Petra Rattue

Source: Medical News Today

ScienceDaily (Feb. 3, 2012) — One of the big mysteries in biology is why cells age. Now scientists at the Salk Institute for Biological Studies report that they have discovered a weakness in a component of brain cells that may explain how the aging process occurs in the brain.

This microscope image shows extremely long-lived proteins, or ELLPs, glowing green on the outside of the nucleus of a rat brain cell. DNA inside the nucleus is pictured in blue. The Salk scientists discovered that the ELLPs, which form channels through the wall of the nucleus, lasted for more than a year without being replaced. Deterioration of these proteins may allow toxins to enter the nucleus, resulting in cellular aging. (Credit: Courtesy of Brandon Toyama, Salk Institute for Biological Studies)

The scientists discovered that certain proteins, called extremely long-lived proteins (ELLPs), which are found on the surface of the nucleus of neurons, have a remarkably long lifespan.

While the lifespan of most proteins totals two days or less, the Salk Institute researchers identified ELLPs in the rat brain that were as old as the organism, a finding they reported February 3 in Science.

The Salk scientists are the first to discover an essential intracellular machine whose components include proteins of this age. Their results suggest the proteins last an entire lifetime, without being replaced.

ELLPs make up the transport channels on the surface of the nucleus; gates that control what materials enter and exit. Their long lifespan might be an advantage if not for the wear-and-tear that these proteins experience over time. Unlike other proteins in the body, ELLPs are not replaced when they incur aberrant chemical modifications and other damage.

Damage to the ELLPs weakens the ability of the three-dimensional transport channels that are composed of these proteins to safeguard the cell’s nucleus from toxins, says Martin Hetzer, a professor in Salk’s Molecular and Cell Biology Laboratory, who headed the research. These toxins may alter the cell’s DNA and thereby the activity of genes, resulting in cellular aging.

Funded by the Ellison Medical Foundation and the Glenn Foundation for Medical Research, Hetzer’s research group is the only lab in the world that is investigating the role of these transport channels, called the nuclear pore complex (NPC), in the aging process.

Previous studies have revealed that alterations in gene expression underlie the aging process. But, until the Hetzer lab’s discovery that mammals’ NPCs possess an Achilles’ heel that allows DNA-damaging toxins to enter the nucleus, the scientific community has had few solid clues about how these gene alterations occur.

"The fundamental defining feature of aging is an overall decline in the functional capacity of various organs such as the heart and the brain," says Hetzer. "This decline results from deterioration of the homeostasis, or internal stability, within the constituent cells of those organs. Recent research in several laboratories has linked breakdown of protein homeostasis to declining cell function."

The results that Hetzer and his team just report suggest that declining neuron function may originate in ELLPs that deteriorate as a result of damage over time.

"Most cells, but not neurons, combat functional deterioration of their protein components through the process of protein turnover, in which the potentially impaired parts of the proteins are replaced with new functional copies," says Hetzer.

"Our results also suggest that nuclear pore deterioration might be a general aging mechanism leading to age-related defects in nuclear function, such as the loss of youthful gene expression programs," he adds.

The findings may prove relevant to understanding the molecular origins of aging and such neurodegenerative disorders as Alzheimer’s disease and Parkinson’s disease.

In previous studies, Hetzer and his team discovered large filaments in the nuclei of neurons of old mice and rats, whose origins they traced to the cytoplasm. Such filaments have been linked to various neurological disorders including Parkinson’s disease. Whether the misplaced molecules are a cause, or a result, of the disease has not yet been determined.

Also in previous studies, Hetzer and his team documented age-dependent declines in the functioning of NPCs in the neurons of healthy aging rats, which are laboratory models of human biology.

Hetzer’s team includes his colleagues at the Salk Institute as well as John Yates III, a professor in the Department of Chemical Physiology of The Scripps Research Institute.

When Hetzer decided three years ago to investigate whether the NPC plays a role in initiating or contributing to the onset of aging and certain neurodegenerative diseases, some members of the scientific community warned him that such a study was too bold and would be difficult and expensive to conduct. But Hetzer was determined despite the warnings.

Source: ScienceDaily

by Jon Cohen on 1 February 2012, 6:00 PM

Synaptic division. Compared with chimpanzees, human children children slowly wire their brains. Credit: Fotosearch

February 3rd, 2012 in Neuroscience 

American scientists believe a new procedure to repair severed nerves could result in patients recovering in days or weeks, rather than months or years. The team used a cellular mechanism similar to that used by many invertebrates to repair damage to nerve axons. Their results are published today in the Journal of Neuroscience Research.

"We have developed a procedure which can repair severed nerves within minutes so that the behavior they control can be partially restored within days and often largely restored within two to four weeks," said Professor George Bittner from the University of Texas. "If further developed in clinical trials this approach would be a great advance on current procedures that usually imperfectly restore lost function within months at best."

The team studied the mechanisms all animal cells use to repair damage to their membranes and focused on invertebrates, which have a superior ability to regenerate nerve axons compared to mammals. An axon is a long extension arising from a nerve cell body that communicates with other nerve cells or with muscles.

This research success arises from Bittner’s discovery that nerve axons of invertebrates which have been severed from their cell body do not degenerate within days, as happens with mammals, but can survive for months, or even years.

The severed proximal nerve axon in invertebrates can also reconnect with its surviving distal nerve axon to produce much quicker and much better restoration of behaviour than occurs in mammals.

"Severed invertebrate nerve axons can reconnect proximal and distal ends of severed nerve axons within seven days, allowing a rate of behavioural recovery that is far superior to mammals," said Bittner. "In mammals the severed distal axonal stump degenerates within three days and it can take nerve growths from proximal axonal stumps months or years to regenerate and restore use of muscles or sensory areas, often with less accuracy and with much less function being restored."

The team described their success in applying this process to rats in two research papers published today. The team were able to repair severed sciatic nerves in the upper thigh, with results showing the rats were able to use their limb within a week and had much function restored within 2 to 4 weeks, in some cases to almost full function.

"We used rats as an experimental model to demonstrate how severed nerve axons can be repaired. Without our procedure, the return of nearly full function rarely comes close to happening," said Bittner. "The sciatic nerve controls all muscle movement of the leg of all mammals and this new approach to repairing nerve axons could almost-certainly be just as successful in humans."

To explore the long term implications and medical uses of this procedure, MD’s and other scientist- collaborators at Harvard Medical School and Vanderbilt Medical School and Hospitals are conducting studies to obtain approval to begin clinical trials.

"We believe this procedure could produce a transformational change in the way nerve injuries are repaired," concluded Bittner.

Provided by Wiley

"New procedure repairs severed nerves in minutes, restoring limb use in days or weeks." February 3rd, 2012. http://medicalxpress.com/news/2012-02-procedure-severed-nerves-minutes-limb.html

February 3, 2012

Schematic drawing of the upright STED microscope used for the experiments. Image: Science, DOI:10.1126/science.1215369

(PhysOrg.com) — Ever since scientists began studying the brain, they’ve wanted to get a better look at what was going on. Researchers have poked and prodded and looked at dead cells under electron microscopes, but never before have they been able to get high resolution microscopic views of actual living brain cells as they function inside of a living animal. Now, thanks to work by physicist Stefan Hell and his colleagues at the Max Planck Institute in Germany, that dream is realized. In a paper published in Science, Hell and his team describe the workings of their marvelous discovery.

Hell (which in German means “bright”) and others at the Institute have been working for years on ultra high resolution microscopes that go by the name “stimulated emission depletion” or STED microscopes. Now, they’ve taken their work to a whole new level by cutting away a small portion of a mouse’s skull and replacing it with a glass window and then placing their latest STED microscope against the glass to peer inside. To make it easier to see what is what, the team first genetically altered the mouse to make certain brain cells fluorescent. Then, to allow for focusing exclusively on just those cells that are lit up, they added software to the microscope to blot out anything that was not lit up. The result is super high resolution real time imagery of the neurons that exist on the exterior part of a living mouse brain. 

(video)

STED time-lapse recording of a single spine at an interval of 10 seconds. The measurement includes 128 z-stacks consisting of 5 slices each. Most of the rapid remodeling of the spine head appears continuous and smooth at this frame rate. No damage is observed at the dendrite or the spine after recording a total of 640 slices. The movie was acquired in a different experiment than the spines in Fig.1. Scale bar = 1µm. Video: DOI:10.1126/science.1215369

The new microscope provides clear resolution down to 70 nanometers, which is four times that ever achieved before and is enough to allow scientists to see the actual movement of dendritic spines, which may help researches understand why they do so.

It is likely that researchers will find many varied uses for the new microscope. One prominent area will almost certainly involve looking into what psychiatric drugs are really doing within synapses, perhaps leading to breakthroughs in pharmaceutical drugs that are better able to target specific illnesses.

One downside to any new scientific breakthrough however, is the natural tendency of many to move from excitation, to wondering about what will come next. In this case, Hell and his team have already started contemplating ideas on ways to allow researchers to study any cell in the living brain at such high resolution, not just those that lie on the surface.

More information: Nanoscopy in a Living Mouse Brain, Science 3 February 2012: Vol. 335 no. 6068 p. 551. DOI: 10.1126/science.1215369

"Renowned physicist invents microscope that can peer at living brain cells." February 3rd, 2012. http://www.physorg.com/news/2012-02-renowned-physicist-microscope-peer-brain.html

ScienceDaily (Feb. 3, 2012) — Placebos reduce pain by creating an expectation of relief. Distraction — say, doing a puzzle — relieves it by keeping the brain busy. But do they use the same brain processes? Neuromaging suggests they do. When applying a placebo, scientists see activity in the dorsolateral prefrontal cortex. That’s the part of the brain that controls high-level cognitive functions like working memory and attention — which is what you use to do that distracting puzzle.

Now a new study challenges the theory that the placebo effect is a high-level cognitive function. The authors — Jason T. Buhle, Bradford L. Stevens, and Jonathan J. Friedman of Columbia University and Tor D. Wager of the University of Colorado Boulder — reduced pain in two ways — either by giving them a placebo, or a difficult memory task. lacebo. But when they put the two together, “the level of pain reduction that people experienced added up. There was no interference between them,” says Buhle. “That suggests they rely on separate mechanisms.” The findings, published in Psychological Science, a journal of the Association for Psychological Science, could help clinicians maximize pain relief without drugs.

In the study, 33 participants came in for three separate sessions. In the first, experimenters applied heat to the skin with a little metal plate and calibrated each individual’s pain perceptions. In the second session, some of the people applied an ordinary skin cream they were told was a powerful but safe analgesic. The others put on what they were told was a regular hand cream. In the placebo-only trials, participants stared at a cross on the screen and rated the pain of numerous applications of heat — the same level, though they were told it varied. For other trials they performed a tough memory task — distraction and placebo simultaneously. For the third session, those who’d had the plain cream got the “analgesic” and vice versa. The procedure was the same.

The results: With either the memory task or the placebo alone, participants felt less pain than during the trials when they just stared at the cross. Together, the two effects added up; they didn’t interact or interfere with each other. The data suggest that the placebo effect does not require executive attention or working memory.

So what about that neuroimaging? “Neuroimaging is great,” says Buhle, “but because each brain region does many things, when you see activation in a particular area, you don’t know what cognitive process is driving it.” This study tested the theory about how placebos work with direct behavioral observation.

The findings are promising for pain relief. Clinicians use both placebos and distraction — for instance, virtual reality in burn units. But they weren’t sure if one might diminish the other’s efficacy. “This study shows you can use them together,” says Buhle, “and get the maximum bang for your buck without medications.”

Source: ScienceDaily

ScienceDaily (Feb. 3, 2012) — When a patient afflicted with schizophrenia hears inner voices something is taking place inside the brain that prevents the individual from perceiving real voices. A simple electronic application may help the patient learn to shift focus.

Image captures of the brain show how neurons are activated in healthy control subjects when hearing actual voices (top row) whereas activation fails to occur in patients who experience auditory hallucinations. (Credit: Kenneth Hugdahl)

"The patient experiences the inner voices as 100 per cent real, just as if someone was standing next to him and speaking" explains Professor Kenneth Hugdahl of the University of Bergen. "At the same time, he can’t hear voices of others actually present in the same room."

Auditory hallucinations are one of the most common symptoms associated with schizophrenia.

Neural activity ceases

Dr Hugdahl’s research group has made use of a variety of neuroimaging techniques, including functional magnetic resonance imaging technology (fMRI) to enable them quite literally to see what happens inside the brain when the inner voices make their presence known. The project received funding under the NevroNor national initiative on neuroscientific research administered under the auspices of the Research Council of Norway

Images of patients’ brains reveal a spontaneous activation of neurons in a particular area of the brain — specifically the rear, upper region of the left temporal lobe. This is the area responsible for speech perception, and when healthy people hear speech it becomes activated. So what happens when patients with schizophrenia hear a real voice and a hallucinatory one at the same time?

"It would be natural to assume that neural activity would increase somewhat — even twofold. But quite the opposite takes place; we actually observed that the activity ceased altogether," states Professor Hugdahl.

Losing contact with the outside world

In order to learn more about what was happening, Hugdahl and his colleagues Kristiina Kompus and René Westerhausen carried out a meta-analysis of 23 studies. These studies focused either on spontaneous inner-voice triggered neural activation in subjects with schizophrenia or the stimulatory reaction prompted by actual sounds in both healthy and schizophrenic subjects.

It emerged that many researchers had observed either that a spontaneous activation of neurons occurs in patients hearing inner voices or that the patients’ perception of actual voices becomes suppressed when these are heard simultaneously with inner voices. No one had seen the connection between these findings.

"Previously, we thought these were two separate phenomena. But our analyses revealed that the one causes the other: when neurons become activated by inner voices it inhibits perception of outside speech. The neurons become ‘preoccupied’ and can’t ‘process’ voices from the outside," explains Professor Hugdahl.

"This may explain why schizophrenic patients close themselves off so completely and lose touch with the outside world when experiencing hallucinations," he purports.

Electronic app designed to improve impulse control

Hugdal and his colleagues made yet another discovery that may well help explain how the lives of these individuals become consumed by inner voices. It turns out that the frontal lobe in the brains of schizophrenia patients does not function exactly the way it should. As a result, these patients have a lesser degree of impulse control and are unable to filter out their inner voices.

"Every one of us hears inner voices or melodies from time to time. The difference between non-afflicted individuals and schizophrenia patients is that the former manage to tune these out better," the professor points out.

If patients could learn to stifle inner noise it could have a huge impact on our ability to treat schizophrenia, he states. To this end, Professor Hugdahl’s research group has developed an application that can be used on mobile phones and other simple electronic devices, to help patients improve their filters.

Wearing headphones, the patient is exposed to simple speech sounds with different sounds played in each ear. The task is to practice hearing the sound in one ear while blocking out sound in the other. The application has only been tested on two patients with schizophrenia so far. The response from these patients is promising, Dr Hugdahl relates.

"The voices are still there, but the test subjects feel that they have control over the voices instead of the other way around. The patient feels it is a breakthrough since it means he can actively shift his focus from the inner voices over to the sounds coming from the outside," the professor explains.

Source: ScienceDaily

Article Date: 03 Feb 2012 - 0:00 PST

We all know that it can take a little while for our hearing to bounce back after listening to our iPods too loud or attending a raucous concert. But new research at the University of Michigan Health System suggests over-exposure to noise can actually cause more lasting changes to our auditory circuitry - changes that may lead to tinnitus, commonly known as ringing in the ears.

U-M researchers previously demonstrated that after hearing damage, touch-sensing “somatosensory” nerves in the face and neck can become overactive, seeming to overcompensate for the loss of auditory input in a way the brain interprets - or “hears” - as noise that isn’t really there.

The new study, which appears in The Journal of Neuroscience, found that somatosensory neurons maintain a high level of activity following exposure to loud noise, even after hearing itself returns to normal.

The findings were made in guinea pigs, but mark an important step toward potential relief for people plagued by tinnitus, says lead investigator Susan E. Shore, Ph.D., of U-M’s Kresge Hearing Research Institute and a professor of otolaryngology and molecular and integrative physiology at the U-M Medical School.

“The animals that developed tinnitus after a temporary loss in their hearing after loud noise exposure were the ones who had sustained increases in activity in these neural pathways,” Shore says. “In the future it may be possible to treat tinnitus patients by dampening the hyperactivity by reprogramming these auditory-touch circuits in the brain.”

In normal hearing, a part of the brain called the dorsal cochlear nucleus is the first stop for signals arriving from the ear via the auditory nerve. But it’s also a hub where “multitasking” neurons process other sensory signals, such as touch, together with hearing information.

During hearing loss, the other sensory signals entering the dorsal cochlear nucleus are amplified, Shore’s earlier research found. This overcompensation by the somatosensory neurons, which carry information about touch, vibration, skin temperature and pain, is believed to fuel tinnitus in many cases.

Tinnitus affects up to 50 million people in the United States and millions more worldwide, according to the American Tinnitus Association. It can range from intermittent and mildly annoying to chronic, severe and debilitating. There is no cure.

It especially affects baby boomers, who, as they reach an age at which hearing tends to diminish, increasingly find that tinnitus moves in. The condition most commonly occurs with hearing loss, but can also follow head and neck trauma, such as after an auto accident, or dental work. Tinnitus is the number one disability afflicting members of the armed forces.

The involvement of touch sensing (or “somatosensory”) nerves in the head and neck explains why many tinnitus sufferers can change the volume and pitch of the sound by clenching their jaw, or moving their head and neck, Shore explains.

While the new study builds on previous discoveries by Shore and her team, many aspects are new.

“This is the first research to show that, in the animals that developed tinnitus after hearing returned to normal, increased excitation from the somatosensory nerves in the head and neck continued. This dovetails with our previous research, which suggests this somatosensory excitation is a major component of tinnitus,” says Shore, who serves on the scientific advisory committee of the American Tinnitus Association.

“The better we understand the underlying causes of tinnitus, the better we’ll be able to develop new treatments,” she adds.

Source: Medical News Today