Category: Disorders and Syndromes

University of Utah scientists used invisible infrared light to make rat heart cells contract and toadfish inner-ear cells send signals to the brain. The discovery someday might improve cochlear implants for deafness and lead to devices to restore vision, maintain balance and treat movement disorders like Parkinson's.

"We're going to talk to the brain with optical infrared pulses instead of electrical pulses," which now are used in cochlear implants to provide deaf people with limited hearing, says Richard Rabbitt, a professor of bioengineering and senior author of the heart-cell and inner-ear-cell studies published this month in The Journal of Physiology.

The studies — funded by the National Institutes of Health — also raise the possibility of developing cardiac pacemakers that use optical signals rather than electrical signals to stimulate heart cells. But Rabbitt says that because electronic pacemakers work well, "I don't see a market for an optical pacemaker at the present time."

The scientific significance of the studies is the discovery that optical signals — short pulses of an invisible wavelength of infrared laser light delivered via a thin, glass optical fiber — can activate heart cells and inner-ear cells related to balance and hearing.

In addition, the research showed infrared activates the heart cells, called cardiomyocytes, by triggering the movement of calcium ions in and out of mitochondria, the organelles or components within cells that convert sugar into usable energy. The same process appears to occur when infrared light stimulates inner-ear cells.

Infrared light can be felt as heat, raising the possibility the heart and ear cells were activated by heat rather than the infrared radiation itself. But Rabbitt and colleagues did "elegant experiments" to show the cells indeed were activated by the infrared radiation, says a commentary in the journal by Ian Curthoys of the University of Sydney, Australia.

Curthoys writes that the research provides "stunningly bright insight" into events within inner-ear cells and "has great potential for future clinical application."

Shedding Infrared Light on Inner-Ear Cells and Heart Cells

The low-power infrared light pulses in the study were generated by a diode — "the same thing that's in a laser pointer, just a different wavelength," Rabbitt says.

The scientists exposed the cells to infrared light in the laboratory. The heart cells in the study were newborn rat heart muscle cells called cardiomyocytes, which make the heart pump. The inner-ear cells are hair cells, and came from the inner-ear organ that senses motion of the head. The hair cells came from oyster toadfish, which are well-establish models for comparison with human inner ears and the sense of balance.

Inner-ear hair cells "convert the mechanical vibration from sound, gravity or motion into the signal that goes to the brain" via adjacent nerve cells, says Rabbitt.

Using infrared radiation, "we were stimulating the hair cells, and they dumped neurotransmitter onto the neurons that sent signals to the brain," Rabbitt says.

He believes the inner-ear hair cells are activated by infrared radiation because "they are full of mitochondria, which are a primary target of this wavelength."

The infrared radiation affects the flow of calcium ions in and out of mitochondria — something shown by the companion study in neonatal rat heart cells.

That is important because for "excitable" nerve and muscle cells, "calcium is like the trigger for making these cells contract or release neurotransmitter," says Rabbitt.

The heart cell study found that an infrared pulse lasting a mere one-5,000th of a second made mitochondria rapidly suck up calcium ions within a cell, then slowly release them back into the cell — a cycle that makes the cell contract.

"Calcium does that normally," says Rabbitt. "But it's normally controlled by the cell, not by us. So the infrared radiation gives us a tool to control the cell. In the case of the [inner-ear] neurons, you are controlling signals going to the brain. In the case of the heart, you are pacing contraction."

New Possibilities for Optical versus Electrical Cochlear Implants

Rabbitt believes the research — including a related study of the cochlea last year — could lead to better cochlear implants that would use optical rather than electrical signals.

Existing cochlear implants convert sound into electrical signals, which typically are transmitted to eight electrodes in the cochlea, a part of the inner ear where sound vibrations are converted to nerve signals to the brain. Eight electrodes can deliver only eight frequencies of sound, Rabbitt says.

"A healthy adult can hear more than 3,000 different frequencies. With optical stimulation, there's a possibility of hearing hundreds or thousands of frequencies instead of eight. Perhaps someday an optical cochlear implant will allow deaf people to once again enjoy music and hear all the nuances in sound that a hearing person would enjoy."

Unlike electrical current, which spreads through tissue and cannot be focused to a point, infrared light can be focused, so numerous wavelengths (corresponding to numerous frequencies of sound) could be aimed at different cells in the inner ear.

Nerve cells that send sound signals from the ears to the brain can fire more than 300 times per second, so ideally, a cochlear implant using infrared light would be able to perform as well. In the Utah experiments, the researchers were able to apply laser pulses to hair cells to make adjacent nerve cells fire up to 100 times per second. For a cochlear implant, the nerve cells would be activated within infrared light instead of the hair cells.

Rabbitt cautioned it may be five to 10 years before the development of cochlear implants that run optically. To be practical, they need a smaller power supply and light source, and must be more power efficient to run on small batteries like a hearing aid.

Optical Prosthetics for Movement, Balance and Vision Disorders

Electrical deep-brain stimulation now is used to treat movement disorders such as Parkinson's disease and "essential tremor, which causes rhythmic movement of the limbs so it becomes difficult to walk, function and eat," says Rabbitt.

He is investigating whether optical rather than electrical deep-brain stimulation might increase how long the treatment is effective.

Rabbitt also sees potential for optical implants to treat balance disorders.

"When we get old, we shuffle and walk carefully, not because our muscles don't work but because we have trouble with balance," he says. "This technology has potential for restoring balance by restoring the signals that the healthy ear sends to the brain about how your body is moving in space."

Optical stimulation also might provide artificial vision in people with retinitis pigmentosa or other loss of retinal cells — the eye cells that detect light and color — but who still have the next level of cells, known as ganglia, Rabbitt says.

"You would wear glasses with a camera [mounted on the frames] and there would be electronics that would convert signals from the camera into pulses of infrared radiation that would be patterned onto the diseased retina that normally does not respond to light but would respond to the pulsed infrared radiation" to create images, he says.

Hearing and vision implants that use optical rather than electrical signals do not have to penetrate the brain or other nerve tissue because infrared light can penetrate "quite a bit of tissue," so devices emitting the light "have potential for excellent biocompatibility," Rabbitt says. "You will be able to implant optical devices and leave them there for life."

The heart cell study was led by Rabbitt, with University of Utah bioengineering doctoral student Gregory Dittami as first author. Co-authors were Suhrud Rajguru, a former Utah doctoral student now at Northwestern University in Chicago; Utah doctoral student Richard Lasher; and Robert Hitchcock, an assistant professor of bioengineering at the University of Utah.

Rabbitt's coauthors on the inner-ear study included first author Rajguru; Dittami; Claus-Peter Richter and Agnella Matic of Northwestern University; neuroscientist Gay Holstein of Mount Sinai School of Medicine in New York; and neuroscientist Stephen Highstein of the Marine Biological Laboratory in Woods Hole, Mass.

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Journal References:

1. Gregory M. Dittami, Suhrud M. Rajguru, Richard A. Lasher, Robert W. Hitchcock, Richard D. Rabbitt. Intracellular calcium transients evoked by pulsed infrared radiation in neonatal cardiomyocytes. The Journal of Physiology, 2011; 589 (6): 1295 DOI: 10.1113/jphysiol.2010.198804
2. Suhrud M. Rajguru, Claus-Peter Richter, Agnella I. Matic, Gay R. Holstein, Stephen M. Highstein, Gregory M. Dittami, Richard D. Rabbitt. Infrared photostimulation of the crista ampullaris. The Journal of Physiology, 2011; 589 (6): 1283 DOI: 10.1113/jphysiol.2010.198333

Looking to spice up your sex life? Try adding ginseng and saffron to your diet. Both are proven performance boosters, according to a new scientific review of natural aphrodisiacs conducted by University of Guelph researchers.

Indulge in wine and chocolate, too, but know that their amorous effects are likely all in your head. Stay away from the more obscure Spanish fly and Bufo toad. While purported to be sexually enhancing, they produced the opposite result and can even be toxic.

Those are among the findings of the study by Massimo Marcone, a professor in Guelph's Department of Food Science, and master's student John Melnyk. The results will appear in the journal Food Research International but are available online now.

"Aphrodisiacs have been used for thousands of years all around the world, but the science behind the claims has never been well understood or clearly reported," Marcone said.

"Ours is the most thorough scientific review to date. Nothing has been done on this level of detail before now." There is a need for natural products that enhance sex without negative side effects, Melnyk added. Currently, conditions such as erectile dysfunction are treated with synthetic drugs, including sildenafil (commonly sold as Viagra) and tadalafil (Cialis).

"But these drugs can produce headache, muscle pain and blurred vision, and can have dangerous interactions with other medications. They also do not increase libido, so it doesn't help people experiencing low sex drive," he said.

The researchers examined hundreds of studies on commonly used consumable aphrodisiacs to investigate claims of sexual enhancement — psychological and physiological.

Ultimately, they included only studies meeting the most stringent controls.

The results? They found that panax ginseng, saffron and yohimbine, a natural chemical from yohimbe trees in West Africa, improved human sexual function.

People report increased sexual desire after eating muira puama, a flowering plant found in Brazil; maca root, a mustard plant in the Andes; and chocolate. Despite its purported aphrodisiac effect, chocolate was not linked to sexual arousal or satisfaction, the study said.

"It may be that some people feel an effect from certain ingredients in chocolate, mainly phenylethylamine, which can affect serotonin and endorphin levels in the brain," Marcone said.

Alcohol was found to increase sexual arousal but to impede sexual performance.

Nutmeg, cloves, garlic, ginger, and ambergris, formed in the intestinal tract of the sperm whale, are among substances linked to increased sexual behaviour in animals.

While their findings support the use of foods and plants for sexual enhancement, the authors urge caution. "Currently, there is not enough evidence to support the widespread use of these substances as effective aphrodisiacs," Marcone said. "More clinical studies are needed to better understand the effects on humans."

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Journal Reference:

1. John P. Melnyk, Massimo F. Marcone. Aphrodisiacs from Plant and Animal Sources – A Review of Current Scientific Literature. Food Research International, 2011; DOI: 10.1016/j.foodres.2011.02.043

The first study to examine the activity of hundreds of individual human brain cells during seizures has found that seizures begin with extremely diverse neuronal activity, contrary to the classic view that they are characterized by massively synchronized activity. The investigation by Massachusetts General Hospital (MGH) and Brown University researchers also observed pre-seizure changes in neuronal activity both in the cells where seizures originate and in nearby cells.

The report will appear in Nature Neuroscience and is receiving advance online publication.

"Our findings suggest that different groups of neurons play distinct roles at different stages of seizures," says Sydney Cash, MD, PhD, of the MGH Department of Neurology, the paper's senior author. "They also indicate that it may be possible to predict impending seizures, and that clinical interventions to prevent or stop them probably should target those specific groups of neurons."

Epileptic seizures have been reported since ancient times, and today 50 million individuals worldwide are affected; but much remains unknown about how seizures begin, spread and end. Current knowledge about what happens in the brain during seizures largely comes from EEG readings, which reflect the average activity of millions of neurons at a time. This study used a neurotechnology that records the activity of individual brain cells via an implanted sensor the size of a baby aspirin.

The researchers analyzed data gathered from four patients with focal epilepsy — seizures that originate in abnormal brain tissues — that could not be controlled by medication. The participants had the sensors implanted in the outer layer of brain tissue to localize the abnormal areas prior to surgical removal. The sensors recorded the activity of from dozens to more than a hundred individual neurons over periods of from five to ten days, during which each patient experienced multiple seizures. In some participants, the recordings detected changes in neuronal activity as much as three minutes before a seizure begins and revealed highly diverse neuronal activity as a seizure starts and spreads. The activity becomes more synchronized toward the end of the seizure and almost completely stops when a seizure ends.

"Even though individual patients had different patterns of neural activity leading up to a seizure, in most of them it was possible to detect changes in that activity before the upcoming seizure," says co-lead and corresponding author Wilson Truccolo, PhD, Brown University Department of Neuroscience and an MGH research fellow. "We're still a long way from being able to predict a seizure — which could be a crucial advance in treating epilepsy — but this paper points a direction forward. For most patients, it is the unpredictable nature of epilepsy that is so debilitating, so just knowing when a seizure is going to happen would improve their quality of life and could someday allow clinicians to stop it before it starts."

Cash adds, "We are using ever more sophisticated methods to handle the large amounts of data we are collecting from patients. Now we are assessing how well we actually can predict seizures using ensembles of single neurons and are continuing to use these advanced recording techniques to unravel the mechanisms that cause human seizures and leveraging this knowledge to make the most of animal models." Cash is an assistant professor of Neurology at Harvard Medical School, and Truccolo an assistant professor of Neuroscience (Research) at Brown.

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Journal Reference:

1. Wilson Truccolo, Jacob A Donoghue, Leigh R Hochberg, Emad N Eskandar, Joseph R Madsen, William S Anderson, Emery N Brown, Eric Halgren, Sydney S Cash. Single-neuron dynamics in human focal epilepsy. Nature Neuroscience, 2011; DOI: 10.1038/nn.2782

A team of Neuroscientists from NeuroCure Cluster of Excellence at Charité — Universitätsmedizin Berlin and Baylor College of Medicine in Houston, Texas, have made a major breakthrough in understanding how signals are processed in the human brain.

The paper, published in the current issue of the scientific journal Neuron, shows that a certain type of protein — the "vesicular glutamate transporter" (VGLUT) plays a crucial part in the strength regulation of synaptic connections. This regulation enables synapses to vary in strength.

Synapses transmit the communication between different neurons within the central nervous system and depending on their function in the brain, they operate differently. For example, the cerebral cortex bundles a vast amount of information and in order to process this, neurons need to dose or regulate the information. Neuroscientist Christian Rosenmund, who moved his lab from Baylor College of Medicine to Charité — Universitätsmedizin Berlin in 2009, has been focusing on the function of synapses for years.

"A neuron can be compared to a music enthusiast. He doesn´t hear the single sounds but the whole concert. Synapses are like single sounds. Some play louder, some play more quietly," he illustrates. But until now scientists did not know how they were regulated. However, a dysfunction of synapses can have a dramatic impact on signal processing in the brain and can lead to neurological diseases. The Rosenmund team has now made a major breakthrough and discovered the regulator for the volume of the nerve cells — the protein endophilin. Its interaction with a certain variety of the glutamate transporter (VGLUT) plays the key role. The widely known 'housekeeping' function of these proteins is to fill vesicles with the neurotransmitter glutamate. That the transporter has a regulating function as well was a big surprise.

"We found a mechanism how the strength of synapses is controlled. The brain can adapt a synapse adequately to different brain functions. This insight can help us to understand a number of neurological diseases like epilepsy and even treat them," explains Rosenmund. In the future the scientists want to investigate further the pathopysiological relevance of glutamate transporters.

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Journal Reference:

1. Matthew C. Weston, Ralf B. Nehring, Sonja M. Wojcik, Christian Rosenmund. Interplay between VGLUT Isoforms and Endophilin A1 Regulates Neurotransmitter Release and Short-Term Plasticity. Neuron, 2011; 69 (6): 1147 DOI: 10.1016/j.neuron.2011.02.002

A group of scientists at Marshall University is conducting research that may someday lead to new treatments for repair of the central nervous system.

Dr. Elmer M. Price, who heads the research team and is chairman of Marshall's Department of Biological Sciences, said his group has identified and analyzed unique adult animal stem cells that can turn into neurons.

Price said the neurons they found appear to have many of the qualities desired for cells being used in development of therapies for slowly progressing, degenerative conditions like Parkinson's disease, Huntington's disease and multiple sclerosis, and for damage due to stroke or spinal cord injury.

According to Price, what makes the discovery especially interesting is that the source of these neural stem cells is adult blood, a readily available and safe source. Unlike embryonic stem cells, which have a tendency to cause cancer when transplanted for therapy, adult stems like those identified in Price's lab are found in the bodies of all living animals and do not appear to be carcinogenic.

"Neural stem cells are usually found in specific regions of the brain, but our observation of neural-like stem cells in blood raises the potential that this may prove to be a source of cells for therapies aimed at neurological disorders," Price added.

So far, the group at Marshall has been able to isolate the unique neural cells from pig blood. Price said pigs are often used as models of human diseases due to their anatomical and physiological similarities to humans. In the future, his lab will work to isolate similar cells from human blood, paving the way for patients to perhaps one day be treated with stem cells derived from their own blood.

The team's research was published in a recent issue of the Journal of Cellular Physiology. The lead author of the article is Dr. Nadja Spitzer, a research associate in Price's lab. Other contributors include Dr. Lawrence M. Grover, associate professor of pharmacology, physiology and toxicology at Marshall's Joan C. Edwards School of Medicine; and Gregory S. Sammons and Heather M. Butts, who were both undergraduate students when the research was conducted.

The study was supported with funding from the National Science Foundation's Experimental Program to Stimulate Competitive Research (EPSCoR) and the National Institutes of Health.

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Journal Reference:

1. Nadja Spitzer, Gregory S. Sammons, Heather M. Butts, Lawrence M. Grover, Elmer M. Price. Multipotent progenitor cells derived from adult peripheral blood of swine have high neurogenic potential in vitro. Journal of Cellular Physiology, 2011; DOI: 10.1002/jcp.22670

Researchers at Mount Sinai School of Medicine have discovered a way that mutations in a gene called LRRK2 may cause the most common inherited form of Parkinson's disease. The study, published online in PLoS ONE, shows that upon specific modification called phosphorylation, LRRK2 protein binds to a family of proteins called 14-3-3, which has a regulatory function inside cells. When there is a mutation in LRRK2, 14-3-3 is impaired, leading to Parkinson's. This finding explains how mutations lead to the development of Parkinson's, providing a new diagnostic and drug target for the disease.

Using one-of-a-kind mouse models developed at Mount Sinai School of Medicine, Zhenyu Yue, PhD, Associate Professor of Neurology and Neuroscience, and his colleagues, found that several common Parkinson's disease mutations — including one called G2019S — disturb the specific phosphorylation of LRRK2.This impairs 14-3-3 binding with varying degrees, depending on the type of mutation.

"We knew that the LRRK2 mutation triggers a cellular response resulting in Parkinson's disease, but we did not know what processes the mutation disrupted," said Dr. Yue. "Now that we know that phosphorylation is disturbed, causing 14-3-3 binding to be impaired, we have a new idea for diagnostic analysis and a new target for drug development."

Dr. Yue's team also identified a potential enzyme called protein kinase A (PKA), responsible for the phosphorylation of LRRK2. Although the exact cellular functions disrupted by these changes are unclear, their study provides a starting point for understanding brain signaling that contributes to the disease. Recent studies have shown that 14-3-3 binds to other proteins implicated in inherited Parkinson's disease and has a neuroprotective function, and when the binding is impaired due to these mutations, the protection may be lost. The findings also demonstrate additional insight into the functional relevance of the LRRK2 and 14-3-3 interaction.

The presence of 14-3-3 in spinal fluid is already used as a biomarker for the presence of neurodegenerative diseases. Further applications of these findings could point to the use of 14-3-3 as a biomarker in testing for Parkinson's disease.

Dr. Yue's team at Mount Sinai includes Xianting Li, PhD, Associate Scientist, and Nina Pan, Associate Researcher; collaborators Brian T. Chait, PhD, and Qing Jun Wang, PhD, from the Rockefeller University; and Yingming Zhao, PhD, and Sangkyu Lee, PhD, from the University of Chicago. Dr. Yue's work is supported by grants from the National Institutes of Health, and The Michael J. Fox Foundation for Parkinson's Research.

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Journal Reference:

1. Xianting Li, Qing Jun Wang, Nina Pan, Sangkyu Lee, Yingming Zhao, Brian T. Chait, Zhenyu Yue. Phosphorylation-Dependent 14-3-3 Binding to LRRK2 Is Impaired by Common Mutations of Familial Parkinson's Disease. PLoS ONE, 2011; 6 (3): e17153 DOI: 10.1371/journal.pone.0017153

Researchers at Concordia University have pioneered a computer-based method to detect epileptic seizures as they occur — a new technique that may open a window on the brain's electrical activity.

Their paper, "A Novel Morphology-Based Classifier for Automatic Detection of Epileptic Seizures," presented at the annual meeting of the Engineering in Medicine and Biology Society, documents the very successful application of this new seizure-detection method.

An epileptic seizure, which is caused by disruptions in the normal electrical activity of the brain, can produce a range of symptoms including convulsions and unconsciousness. To learn more about the timing and nature of seizures, the electrical activity of patients' brains is often recorded using electroencephalograms (EEGs). At the moment, however, epilepsy experts must review these recordings manually — a time-consuming process.

"EEG recordings may cover a period of several weeks," explains study co-author Rajeev Agarwal, a professor in Concordia's Department of Electrical and Computer Engineering. "That's a lot of data to review. Automating the process is difficult, because there's no exact definition for a seizure, so there's no template to look for. Every seizure is different with every patient."

However, seizures have certain recognizable characteristics. They occur when neurons fire in a synchronous or rhythmic manner. As seizures progress, the EEG signals have very strong transitions. Seen on an EEG recording, the waves of electrical activity tend to be spike-like.

The Concordia team, led by PhD candidate and lead author Rajeev Yadav, devised an algorithm to check the sharpness of the electrical signals on the EEG recordings as measured by their angle or slope. A series of sharp signals indicate a seizure.

This approach proved extremely successful. In the study of EEG recordings of seven patients, the new method detected every seizure while scoring an extremely low rate of false positives. Results are far better than those obtained with existing methods.

This method of detecting seizures may have applications beyond epilepsy. "Patterns of sharp electrical activity in the brain are generally not a good thing," says Agarwal, who is also co-founder, chief technical officer and vice-president of Leap Medical Inc.

"Think of comatose patients in the ICU for example," he continues. "Some of them may be having seizures or epileptic form like activity, but there's no way to know at the moment. Our method may allow health professionals to gain a much clearer picture of patients' brain function."

The research team continues to evaluate and refine this method of seizure detection. More patient data from several different centres is being reviewed, and further publications on the subject are planned. So far, according to Agarwal, results are promising.

This research was supported by the Natural Sciences and Engineering Research Council of Canada and the Regroupement Stratégique en Microsystèmes du Québec.

Patrick Stroman's work mapping the function and information processing of the spinal cord could improve treatment for spinal cord injuries.

"Basic physiology books describe the spinal cord as a relay system, but it's part of the central nervous system and processes information just like parts of the brain do," explains Dr. Stroman, director of the Queen's MRI Facility and Canada Research Chair in Imaging Physics.

Dr. Stroman's research is directed at precisely mapping the areas above and below a spinal cord injury in order to better determine the precise nature of an injury and the effectiveness of subsequent treatment. When medical research has advanced to a point where clinicians are able to bridge an injury on a spinal cord, Dr. Stroman's spinal mapping technique will be key in accurately pinpointing the injury to be bridged.

The technique involves capturing multiple images of the spinal cord using a conventional MRI system. The image capturing is repeated every few seconds over several minutes. During the imaging temperature sensations on the skin are varied allowing areas of the spinal cord that respond to the temperature changes to be detected in the MRI.

During their research, Dr. Stroman's team was also surprised to discover that levels of attention impact information processing in the spinal cord. By examining the differences in spinal cord functioning in people who were either alert or distracted by a task they were able to see changes in the level of cord activity picked up by the MRI scanner.

"The effect of attention is one of the reasons that when you're playing sports and you get hurt, you often don't become aware of the injury until after the game when your attention and focus changes," says Dr. Stroman. "We already knew that a person's level of attention affects information processing in the brain, but this finding has made us aware that level of attention has to be properly controlled in research that aims to accurately map spinal cord function."

Dr. Stroman's spinal cord mapping research has important implications for those with spinal cord injuries who suffer from chronic pain. The research also applies to any conditions — including multiple sclerosis, fibromyalgia, or congenital conditions — where the function of the spinal cord is affected.

Stress can change the balance of bacteria that naturally live in the gut, according to research published this month in the journal Brain, Behavior, and Immunity.

"These bacteria affect immune function, and may help explain why stress dysregulates the immune response," said lead researcher Michael Bailey.

Exposure to stress led to changes in composition, diversity and number of gut microorganisms, according to scientists from The Ohio State University. The bacterial communities in the intestine became less diverse, and had greater numbers of potentially harmful bacteria, such as Clostridium.

"These changes can have profound implications for physiological function," explained Dr Bailey. "When we reduced the number of bacteria in the intestines using antibiotics, we found that some of the effects of stress on the immune system were prevented," he added. "This suggests that not only does stress change the bacteria levels in the gut, but that these alterations can, in turn, impact our immunity."

"This is the first evidence that the gut microorganisms may play a role in innate immunological stress responses," said Monika Fleshner, Professor of Integrative Physiology at the University of Colorado, Boulder. "The study reveals the dynamic interactions between multiple physiological systems including the intestinal microbiota and the immune system."

Because gut bacteria have been linked to diseases like inflammatory bowel disease, and even to asthma, a future goal of the study is to determine whether alterations of gut bacteria is the reason why these diseases tend to be worse during periods of pressure.

The research was conducted with colleagues from the Texas Tech University Health Sciences Center and the Research and Testing Laboratories, and was funded by the National Institute of Health.

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Journal Reference:

1. Bailey. Exposure to a social stressor alters the structure of the intestinal microbiota: Implications for stressor-induced immunomodulation?Brain, Behavior, and Immunity, 2011; 25 (3): 397 DOI: 10.1016/j.bbi.2010.10.023