Synapses are modified through learning. Up until now, scientists believed that a particular form of synaptic plasticity in the brain’s hippocampus was responsible for learning spatial relations. This was based on a receptor type for the neurotransmitter glutamate: the NMDA receptor. Researchers at the Max Planck Institute for Medical Research in Heidelberg and Oxford University have now observed that mice develop a spatial memory, even when the NMDA receptor-transmitted plasticity is switched off in parts of their hippocampus. However, if these mice have to resolve a conflict while getting their bearings, they are not successful in resolving it; the hippocampal NMDA receptors are clearly needed to detect or resolve the conflict. This has led the researchers involved in this experiment to refute a central tenet of neuroscience regarding the function of hippocampal NMDA receptor-transmitted plasticity in spatial learning.
Source: Max Planck Institute for Medical Research
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ScienceDaily (July 19, 2012) — A joint study carried out by The University of Nottingham and the multinational food company Unilever has found for the first time that fat in food can reduce activity in several areas of the brain which are responsible for processing taste, aroma and reward.
The research, now available in the Springer journal Chemosensory Perception, provides the food industry with better understanding of how in the future it might be able to make healthier, less fatty food products without negatively affecting their overall taste and enjoyment. Unveiled in 2010, Unilever’s Sustainable Living Plan sets out its ambition to help hundreds of millions of people improve their diet around the world within a decade.
This fascinating three-year study investigated how the brains of a group of participants in their 20s would respond to changes in the fat content of four different fruit emulsions they tasted while under an MRI scanner. All four samples were of the same thickness and sweetness, but one contained flavour with no fat, while the other three contained fat with different flavour release properties.
The research found that the areas of the participants’ brains which are responsible for the perception of flavour — such as the somatosensory cortices and the anterior, mid & posterior insula — were significantly more activated when the non-fatty sample was tested compared to the fatty emulsions despite having the same flavour perception. It is important to note that increased activation in these brain areas does not necessarily result in increased perception of flavour or reward.
Dr Joanne Hort, Associate Professor in Sensory Science at The University of Nottingham said: “This is the first brain study to assess the effect of fat on the processing of flavour perception and it raises questions as to why fat emulsions suppress the cortical response in brain areas linked to the processing of flavour and reward. It also remains to be determined what the implications of this suppressive effect are on feelings of hunger, satiety and reward.”
Unilever food scientist Johanneke Busch, based at the company’s Research & Development laboratories in Vlaardingen, Netherlands added: “There is more to people’s enjoyment of food than the product’s flavour — like its mouthfeel, its texture and whether it satisfies hunger, so this is a very important building block for us to better understand how to innovate and manufacture healthier food products which people want to buy.”
Source: Science Daily
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July 19, 2012 By Emily Martinez
(Medical Xpress) — UT Dallas researchers recently demonstrated how nerve stimulation paired with specific experiences, such as movements or sounds, can reorganize the brain. This technology could lead to new treatments for stroke, tinnitus, autism and other disorders.
Dr. Michael Kilgard helped lead a team that paired vagus nerve stimulation with physical movement to improve brain function.
In a related paper, UT Dallas neuroscientists showed that they could alter the speed at which the brain works in laboratory animals by pairing stimulation of the vagus nerve with fast or slow sounds.
A team led by Dr. Robert Rennaker and Dr. Michael Kilgard looked at whether repeatedly pairing vagus nerve stimulation with a specific movement would change neural activity within the laboratory rats’ primary motor cortex. To test the hypothesis, they paired the vagus nerve stimulation with movements of the forelimb in two groups of rats. The results were published in a recent issue of Cerebral Cortex.
After five days of stimulation and movement pairing, the researchers examined the brain activity in response to the stimulation. The rats who received the training along with the stimulation displayed large changes in the organization of the brain’s movement control system. The animals receiving identical motor training without stimulation pairing did not exhibit any brain changes, or plasticity.
People who suffer strokes or brain trauma often undergo rehabilitation that includes repeated movement of the affected limb in an effort to regain motor skills. It is believed that repeated use of the affected limb causes reorganization of the brain essential to recovery. The recent study suggests that pairing vagus nerve stimulation with standard therapy may result in more rapid and extensive reorganization of the brain, offering the potential for speeding and improving recovery following stroke, said Rennaker, associate professor in The University of Texas at Dallas’ School of Behavioral and Brain Sciences.
“Our goal is to use the brain’s natural neuromodulatory systems to enhance the effectiveness of standard therapies,” Rennaker said. “Our studies in sensory and motor cortex suggest that the technique has the potential to enhance treatments for neurological conditions ranging from chronic pain to motor disorders. Future studies will investigate its effectiveness in treating cognitive impairments.”
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July 19, 2012
(Medical Xpress) — When learning to master complex movements such as those required in surgery, is being physically guided by an expert more effective than learning through trial and error?
Dr. George Van Doorn and a participant in the fMRI
New research by Monash University’s Departments of Psychological Studies and Physiology challenges earlier claims that externally guided (or passive) movement is a superior learning method to self-generated (or active) movement.
In the first study of its kind, researchers discovered that different brain regions become active depending on the type of movement used. Lead researcher Dr. George Van Doorn, head of Psychological Studies, said the findings did not support the view that passive movement was a more effective way to learn.
“There has been much debate over the last 30 years about which form of movement is better,” Dr. Van Doorn said. “We found that active movements result in greater activation in brain areas implicated in higher-order processes such as monitoring and controlling goal-directed behaviour, attention, execution of movements, and error detection.
“Passive movements, in contrast, produced greater activity in areas associated with touch perception, length discrimination, tactile object recognition, and the attenuation of sensory inputs.”
People were tested while making movements themselves, and while being guided.
“Whilst inside a functional Magnetic Resonance Imaging (fMRI) machine, we had people either freely move their index finger around a two-dimensional, raised-line pattern to measure self-generated touch. Or we had an experimenter guide the person’s finger around the pattern, to measure externally generated touch. Using the fMRI, we found that different brain regions become active depending on the type of movement used,” Dr. Van Doorn said.
Dr. Van Doorn said touch was becoming a popular area of investigation, with more scientists contributing to understanding about this important, though under-acknowledged, sensory system.
All researchers involved in this study are located at Monash University’s Gippsland campus. The study findings were presented at EuroHaptics 2012, a major international conference and the primary European meeting for researchers in the field of human haptic sensing and touch-enabled computer applications.
Provided by Monash University
Source: medicalxpress.com
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ScienceDaily (July 19, 2012) — By decoding brain activity, scientists were able to “see” that two monkeys were planning to approach the same reaching task differently — even before they moved a muscle.
The obstacle-avoidance task is a variation on the center-out reaching task in which an obstacle sometimes prevents the monkey from moving directly to the target. The monkey must first place a cursor (yellow) on the central target (purple). This was the starting position. After the first hold, a second target appeared (green). After the second hold an obstacle appeared (red box). After the third hold, the center target disappeared, indicating a “go” for the monkey, which then moved the cursor out and around the obstacle to the target. (Credit: Moran/Pearce)
Anyone who has looked at the jagged recording of the electrical activity of a single neuron in the brain must have wondered how any useful information could be extracted from such a frazzled signal.
But over the past 30 years, researchers have discovered that clear information can be obtained by decoding the activity of large populations of neurons.
Now, scientists at Washington University in St. Louis, who were decoding brain activity while monkeys reached around an obstacle to touch a target, have come up with two remarkable results.
Their first result was one they had designed their experiment to achieve: they demonstrated that multiple parameters can be embedded in the firing rate of a single neuron and that certain types of parameters are encoded only if they are needed to solve the task at hand.
Their second result, however, was a complete surprise. They discovered that the population vectors could reveal different planning strategies, allowing the scientists, in effect, to read the monkeys’ minds.
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Cajal’s histological preparations and drawings showing some contributions to glial cells. (A) Fibrous astrocyte in the white matter of adult brain (formalin-uranium nitrate and gold-sublimated chloride); (B) Protoplasmic astrocyte in an adult brain (silver carbonate (del Rio) and formalin-uranium nitrate); (C) Twin astrocytes in the human hippocampus (formalin-uranium nitrate); (D) Fibrous astrocytes from the white substance of adult brain (Golgi methods); (E) Olygodendrocytes (ammoniacal silver oxide and Nissl); (F) Microglia cells (ammoniacal silver oxide, reduced silver nitrate and silver carbonate (del Rio) methods).
Source: The Histological Slides and Drawings of Cajal
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More than 125 years ago, Santiago Ramón y Cajal was able to draft and prove the neuron doctrine, and later, to develop prophetic theories about neural function and plasticity, many of which have been proven by current neuroscience.
It was chance that made Cajal, during his doctorate studies, have his first contact with histology and force him to study the then current theories about pathogenesis of inflammation.
Thus, he gained knowledge of the vascular hypothesis, by Julius Cohnheim, a German pathologist who, opposing the opinion of his teacher and father of cellular pathology, Rudolf Virchow, made leukocytes the protagonists of inflammation, given their ability to develop ameboid movements directed by chemical signals. Cohnheim’s chemotactic theory deeply influenced Cajal’s conception of biology. So, the basic postulates of chemotaxis can be identified at different moments in Cajal’s research, from the description of the “growth cone” in embryonic neuroblasts, the origin of the neurotrophic theory, to the proposal of the pathophysiological mechanisms of neuronal plasticity.
From Cajal’s point of view, the neurons move during their development and also adapt to different external circumstances. Chemical endogenous substances can stimulate this movement in a similar way to leukocytes during the process of inflammation.
Source: Neuroscience, Volume 217, Pages 1-5 (16 August 2012)
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A: Fueling all this brain activity, and the basis for some imaging techniques, is a dense network of delicate blood vessels.
B: Neurons communicate with one another by releasing chemicals, such as dopamine, from pouches called vesicles. The vesicles, seen here in a fibroblast cell, have a geodesic outer coating that eventually pops through the side of the cell and releases its chemical message to be detected by the cell’s neighbors.
C: Our cells are surrounded by a scaffold of proteins that maintains a cell’s shape. Under an electron microscope, protein fibers called actin filaments look like braided ropes.
D: A few years ago, neuroscientists figured out how to take two fluorescent proteins that glowed in green or red and turn them into a rainbow of different colors that can be incorporated into individual neurons. Here the technique is used to stain cells in the cerebellum. The result? A “brainbow.”
Source: Portraits of the Mind: Visualizing the Brain from Antiquity to the 21st Century
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ScienceDaily (July 18, 2012) — Researchers at Oregon Health & Science University School of Dentistry have discovered that TDP-43, a protein strongly linked to ALS (amyotrophic lateral sclerosis) and other neurodegenerative diseases, appears to activate a variety of different molecular pathways when genetically manipulated. The findings have implications for understanding and possibly treating ALS and neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
ALS affects two in 100,000 adults in the United States annually and the prognosis for patients is grim.The new discovery is published online in G3: Genes, Genomes, Genetics (and the July 2012 print issue of G3).
Using a fruit fly model, the OHSU team genetically increased or eliminated TDP-43 to study its effect on the central nervous system. By using massively parallel sequencing methods to profile the expression of genes in the central nervous system, the team found that the loss of TDP-43 results in widespread gene activation and altered splicing, much of which is reversed by rescue of TDP-43 expression. Although previous studies have implicated both absence and over expression of TDP-43 in ALS, the OHSU study showed little overlap in the gene expression between these two manipulations, suggesting that the bulk of the genes affected are different.
"Our data suggest that TDP-43 plays a role in synaptic transmission, synaptic release and endocytosis," said Dennis Hazelett, Ph.D., lead author of the study. "We also uncovered a potential novel regulation of several pathways, many targets of which appear to be conserved."
Source: Science Daily
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ScienceDaily (July 18, 2012) — Researchers from the University of Medicine and Dentistry of New Jersey (UMDNJ), collaborating with scientists from Northwestern University in Illinois, have provided direct experimental evidence that diabetes is linked to the onset of Alzheimer’s disease. The study, published online this week in the Journal of Alzheimer’s Disease, used an experimental model that shows potential as an important new tool for investigations of Alzheimer’s disease and of drugs being developed to treat Alzheimer’s.
UMDNJ researchers Peter Frederikse, PhD, and Chinnaswamy Kasinathan, PhD, collaborated with William Klein, PhD, at Northwestern University, to build on prior studies from the Klein lab and others that indicated close links between Alzheimer’s disease and diabetes. Working with Claudine Bitel and Rajesh Kaswala, students at UMDNJ, the researchers tested whether untreated diabetes would provide a physiological model of Alzheimer neuropathology.
"The results were striking," Frederikse said. "Because we used diabetes as an instigator of the disease, our study shows — for the first time directly — the link between Alzheimer’s and diabetes."
The researchers found substantial increases in amyloid beta peptide pathology — a hallmark of Alzheimer’s disease — in the brain cortex and hippocampus concurrent with diabetes. They also found significant amyloid beta pathology in the retina and by contrast, when diabetes is not present, no observable pathology was detected in either the brain or the retina.
"Second, our study examined the retina, which is considered an extension of the brain, and is more accessible for diagnostic exams," Frederikse added. "Our findings indicate that scientists may be able to follow the onset and progression of Alzheimer’s disease through retinal examination, which could provide a long sought after early-warning sign of the disease."
This experimental model replicated spontaneous formation of amyloid beta “oligomer” assemblies in brain and retina which may help to explain one of the most widely recognized symptoms of Alzheimer’s. “This is exciting,” Klein said. “Oligomers are the neurotoxins now regarded as causing Alzheimer’s disease memory loss. What could cause them to appear and buildup in late-onset Alzheimer’s disease has been a mystery, so these new findings with diabetes represent an important step.”
Previous research indicated that insulin plays an important role in the formation of memories. Once attached to neurons, oligomers cause insulin receptors to be eliminated from the surface membranes, contributing to insulin resistance in the brain. This launches a vicious cycle in which diabetes induces oligomer accumulation which makes neurons even more insulin resistant.
"In light of the near epidemic increases in Alzheimer’s disease and diabetes today, developing a physiological model of Alzheimer neuropathology has been an important goal," Kasinathan added. "It allows us to identify a potential biomarker for Alzheimer’s disease and may also make important contributions to Alzheimer drug testing and development."
Source: Science Daily
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