Posts tagged brain
Articles and news from the latest research reports.
Light on the Brain
By Sabrina Richards | September 20, 2012
Researchers find that photoreceptors expressed in zebrafish hypothalamus contribute to light-dependent behavior.
Juvenile zebrafish.
Zebrafish larvae without eyes or pineal glands can still respond to light using photopigments located deep within their brains. Published in Current Biology, the findings are the first to link opsins, photoreceptors located in the hypothalamus and other brain areas, to increased swimming in response to darkness, a behavior researchers hypothesize may help the fish move toward better-lit environments.
“[It’s a] strong demonstration that opsin-dependent photoreceptors in deep brain areas affect behaviors,” said Samer Hattar, who studies light reception in mammals at Johns Hopkins University but did not participate in the research.
Photoreceptors in eyes enable vision, and photoreceptors in the pineal gland, a small endocrine gland located in the center of the vertebrate brain, regulate circadian rhythms. But photoreceptors are also found in other brain areas of both invertebrates and vertebrate lineages. The function of these extraocular photoreceptors has been best studied in birds, where they regulate seasonal reproduction, explained Harold Burgess, a behavioral neurogeneticist at the Eunice Kennedy Shriver National Institute for Child Health and Human Development.
Many opsins have been reported in the brains of tiny and transparent larval zebrafish, raising the possibility that light could be stimulating the photoreceptors even deep in the brain. To test for behaviors that may be regulated by deep brain photoreceptors, Burgess and his colleagues in Wolfgang Driever’s lab at the University of Freiburg removed the eyes of zebrafish larvae, and compared their behavior to larvae that retained their eyes. Although most light-dependent behavior required eyes, the eyeless larvae did respond when the lights were turned off, increasing their activity for a several minutes, though to a somewhat lesser extent than control larvae. But the fact that they responded at all suggests that non-retinal photoreceptors contributed to the behavior.
To confirm the role of the deep brain photoreceptors, the researchers also tested eyeless larvae that had been genetically modified to block expression of photoreceptors in the pineal gland. This fish still showed this jump in activity for several minutes after entering darkness.
Two different types of opsins—melanopsin and multiple tissue opsin—are expressed in the same type of neuron in zebrafish hypothalamus. Burgess and his colleagues looked at zebrafish missing the transcription factor Orthopedia, which is unique to these neurons, and found that the darkness-induced activity boost is nearly absent in these fish. To further narrow the search for the responsible photoreceptors, the researchers overexpressed melanopsin in hypothalamus neurons that co-express Orthopedia and melanopsin, and found that it increased the sensitivity of eyeless zebrafish to reductions in light. The results point to both melanopsin and Orthopedia as key players in modulating this behavior and pinpoint the location to neurons that coexpress these factors in the zebrafish hypothalamus.
Interestingly, the hypothalamus is one of the oldest parts of the vertebrate brain, said Detlev Arendt, a developmental biologist at the European Molecular Biology Laboratory in Heidelberg. “It’s very possible that this is one of the oldest functions”—one that evolved in “non-visual organisms” that had no eyes but still needed to sense light.
Although not as directed and efficient as eye-dependent behaviors that help fish swim toward light, Burgess speculates that deep brain opsins can still benefit zebrafish larvae. “You could imagine situation where it can’t see light, if a leaf falls on it and it doesn’t know where to swim. I think this behavior puts it in a hyperactive state where it swims wildly for several minutes until it reaches enough light for eyes to take over,” he explained, noting that such behavior is common in invertebrates.
It remains to be seen whether these deep brain opsins regulate other behaviors, perhaps in similar fashion to seasonal hormonal regulation in birds, but Hattar believes it is likely. “It’s beyond reasonable doubt there are many functions for these deep brain photoreceptors.”
(Source: the-scientist.com)
Study reveal brain cells’ weakest links
People with degenerative neurological conditions could benefit from research that shows why their brain cells stop communicating properly.
Scientists believe that the findings could help to develop treatments that slow the progress of a broad range of brain disorders such as Huntington’s, Alzheimer’s and Parkinson’s diseases.
The team at the University, led by Professor Tom Gillingwater, analysed how connection points between brain cells break down during disease and identified six proteins that control the process.
Sending Signals
When connection points in the brain, known as synapses, stop working - because of injury or disease - the chain of brain signalling breaks down and cannot be repaired.
The research from The Roslin Institute and Centre for Integrative Physiology at the University will help scientists identify drugs that target these proteins.
This could eventually enable clinicians to slow the progress of these disorders.
This study has identified key proteins that may control what goes wrong in a range of brain disorders. We now hope to identify drugs that prevent the breakdown of communication between brain cells and, as a result, halt the progress of these devastating neurodegenerative conditions. — Dr Thomas Wishart Career Track Fellow, The Roslin Institute at the University
(Source: ed.ac.uk)
Understanding the Chemical Mechanism Behind Antidepressants
Millions of Americans take antidepressants such as Prozac, Effexor, and Paxil, but the explanations for how they work never satisfied René Hen, a professor of psychiatry, neuroscience and pharmacology.
So the French-born researcher began a series of experiments a decade ago that are now helping to overturn conventional wisdom about the class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) and providing new insights into the biological mechanisms in the brain that affect mood and cognition.
Adult-born neurons in the hippocampus have been engineered to express channelrhodopsin (red), a protein that allows the activation of these neurons and the study of their impact on pattern separation and mood. (Image credit: Mazen Kheirbek and René Hen)
SSRIs, it has long been thought, work by inhibiting brain cells from reabsorbing serotonin, a signaling agent in the brain associated with positive mood. Yet unlike with psychoactive substances, the effects of the drugs take weeks to be felt—even though the increase in serotonin circulating in the brain begins almost immediately. Something more, Hen concluded, must be happening after that to create such a profound effect in depressed patients.
In 2003, Hen demonstrated an important finding in mice: The change in mood—measured by the amount of time it took the animals to overcome anxiety and feed in new environments—appeared to be due in part to the production of new brain cells in the hippocampus, an area of the brain associated with learning and memory. And those new brain cells, Hen thinks, are the result of growth-stimulating chemicals released in the brain, in response to the increased serotonin.
Last year, Hen published another groundbreaking study, suggesting how these new brain cells might affect mood. The new brain cells are located in the dentate gyrus, an area of the hippocampus involved in pattern separation, a cognitive process that helps us to recognize that something is new and different from similar experiences and stimuli. This information is then sent to other brain regions where the new stimulus is assigned a positive or negative emotional value.
Using genetic manipulations that block or enhance the production of brain cells in the dentate gyrus, Hen demonstrated that the new brain cells led to a marked improvement not just in the cognitive abilities of mice, but also in their mood. “What we think, even though it hasn’t been proven yet, is that some depressed human patients also have a problem with pattern separation,” Hen says. “What we are hoping is, if we can boost production of new neurons in their hippocampus, maybe we can improve pattern separation in patients and decrease general symptoms.”
Hen sees numerous ways that a disruption in pattern separation might lead to negative emotions such as anxiety and depression. The hippocampus is located next to, and is strongly linked with, another brain structure, the almond-shaped amygdala, thought to be the seat of our emotions.
If wrong judgments were assigned to novel stimuli in the amygdala, that could easily trigger the brain’s fight-or-flight instinct or, at the very least, produce fear. That might help explain features of anxiety disorders—why survivors of the 9/11 terrorist attacks suffering from post-traumatic stress disorder, for instance, might be hit with a panic attack whenever they see an airplane fly over a skyscraper, Hen says.
A deficit in pattern separation might also help explain why depressed patients often are unable to experience pleasure, exhibit a lack of interest in novel experiences, and feel profound malaise. Perhaps they are simply unable to register an experience as novel or pleasurable because they are unable to recognize it as sufficiently different from prior experiences.
Hen is quick to point out that new brain cell production in the hippocampus is just one effect of a cascade of neurochemical changes unleashed by SSRIs. Other researchers have demonstrated, among other things, that the drugs also have a strong impact on the prefrontal cortex, the area of the brain associated with executive functions such as decision-making and restraint.
Even so, Hen hopes his findings will have significant implications for some depressed patients—and perhaps even reveal why certain antidepressants work for some people and not others. Over the next several years, he plans to explore his hypotheses further by evaluating the pattern-separation abilities of depressed patients before and after they are treated with SSRIs.
“There is still a long way to go, but we are at least starting to provide a theoretical framework,” Hen says. “With complex disorders such as anxiety and depression, you are dealing with many parts of the brain. We think we have identified the biological basis for one of the symptoms present in a subgroup of patients, and maybe by targeting it, we will be able to help them.”
(Source: news.columbia.edu)
Bumblebees are anything but bumbling: The insects quickly figure out the optimal route for visiting five far-flung flowers, a computational task that even human brains find challenging.
That result suggests that an elaborate mental map isn’t necessary to travel efficiently in unknown territory. Finding a way to mimic the bumblebee’s navigation system may allow programmers to develop robots that adeptly maneuver through unfamiliar places.
The new study, published online September 20 in PLOS Biology, pulls together several lines of previous research into one grand experiment. After training bumblebees to associate artificial flowers with a reward, scientists from the University of Sydney, Rothamsted Research in Harpenden, England and Queen Mary University of London arranged five flowers in a pentagon with sides 50 meters long. One at a time, bumblebees outfitted with a little radar antenna were released from the nest. The bees’ movements were tracked by radar, and motion-sensing cameras on the flowers recorded each visiting bee.
A computer analysis of the bees’ movements suggested that the insects were doing some quick comparing. If a bee went from flower A to B and later went from flower A to C, it would compare those routes, adding the one that was shorter to its itinerary and abandoning longer paths. The bees also made adjustments when a flower was moved to a different location. These results suggest that bees don’t need a big-picture map to search their surroundings, says team member Mathieu Lihoreau, a behavioral ecologist at the University of Sydney.
“It’s amazing that these little creatures are as flexible as they are and have evolved these solutions that make maximum use of these little brains they are carrying around,” says behavioral biologist Fred Dyer of Michigan State University in East Lansing.
![Study suggests that a poor sense of smell may be a marker for psychopathic traits.
People with psychopathic tendencies have an impaired sense of smell, which points to inefficient processing in the front part of the brain [orbitofrontal cortex]. These findings by Mehmet Mahmut and Richard Stevenson, from Macquarie University in Australia, are published online in Springer’s journal Chemosensory Perception.
Psychopathy is a broad term that covers a severe personality disorder characterized by callousness, manipulation, sensation-seeking and antisocial behaviors, traits which may also be found in otherwise healthy and functional people. Studies have shown that people with psychopathic traits have impaired functioning in the front part of the brain – the area largely responsible for functions such as planning, impulse control and acting in accordance with social norms. In addition, a dysfunction in these areas in the front part of the brain is linked to an impaired sense of smell.
Mahmut and Stevenson looked at whether a poor sense of smell was linked to higher levels of psychopathic tendencies, among 79 non-criminal adults living in the community. First they assessed the participants’ olfactory ability as well as the sensitivity of their olfactory system. They also measured subjects’ levels of psychopathy, looking at four measures: manipulation; callousness; erratic lifestyles; and criminal tendencies. They also noted how much or how little they emphasized with other people’s feelings.
The researchers found that those individuals who scored highly on psychopathic traits were more likely to struggle to both identify smells and tell the difference between smells, even though they knew they were smelling something. These results show that brain areas controlling olfactory processes are less efficient in individuals with psychopathic tendencies.](http://41.media.tumblr.com/tumblr_map26zYKw21rog5d1o1_500.jpg)
Study suggests that a poor sense of smell may be a marker for psychopathic traits.
People with psychopathic tendencies have an impaired sense of smell, which points to inefficient processing in the front part of the brain [orbitofrontal cortex]. These findings by Mehmet Mahmut and Richard Stevenson, from Macquarie University in Australia, are published online in Springer’s journal Chemosensory Perception.
Psychopathy is a broad term that covers a severe personality disorder characterized by callousness, manipulation, sensation-seeking and antisocial behaviors, traits which may also be found in otherwise healthy and functional people. Studies have shown that people with psychopathic traits have impaired functioning in the front part of the brain – the area largely responsible for functions such as planning, impulse control and acting in accordance with social norms. In addition, a dysfunction in these areas in the front part of the brain is linked to an impaired sense of smell.
Mahmut and Stevenson looked at whether a poor sense of smell was linked to higher levels of psychopathic tendencies, among 79 non-criminal adults living in the community. First they assessed the participants’ olfactory ability as well as the sensitivity of their olfactory system. They also measured subjects’ levels of psychopathy, looking at four measures: manipulation; callousness; erratic lifestyles; and criminal tendencies. They also noted how much or how little they emphasized with other people’s feelings.
The researchers found that those individuals who scored highly on psychopathic traits were more likely to struggle to both identify smells and tell the difference between smells, even though they knew they were smelling something. These results show that brain areas controlling olfactory processes are less efficient in individuals with psychopathic tendencies.
Plasticity of Inhibition
Until recently, the study of plasticity of neural circuits focused almost exclusively on potentiation and depression at excitatory synapses on principal cells. Other elements in the neural circuitry, such as inhibitory synapses on principal cells and the synapses recruiting interneurons, were assumed to be relatively inflexible, as befits a role of inhibition in maintaining stable levels and accurate timing of neuronal activity. It is now evident that inhibition is highly plastic, with multiple underlying cellular mechanisms. This Review considers these recent developments, focusing mainly on functional and structural changes in GABAergic inhibition of principal cells and long-term plasticity of glutamateric recruitment of inhibitory interneurons in the mammalian forebrain. A major challenge is to identify the adaptive roles of these different forms of plasticity, taking into account the roles of inhibition in the regulation of excitability, generation of population oscillations, and precise timing of neuronal firing.
How do language families evolve over many thousands of years? How stable over time are structural features of languages? Dan Dediu and Stephen Levinson from the Max Planck Institute for Psycholingustics in Nijmegen introduced a new method using Bayesian phylogenetic approaches to analyse the evolution of structural features in more than 50 language families. Their paper ‘Abstract profiles of structural stability point to universal tendencies, family-specific factors, and ancient connections between languages’ was published online on September 20, 2012 in PLoS ONE.
Brain study reveals the roots of chocolate temptations
Researchers have new evidence in rats to explain how it is that chocolate candies can be so completely irresistible. The urge to overeat such deliciously sweet and fatty treats traces to an unexpected part of the brain and its production of a natural, opium-like chemical, according to a report published online on September 20th in Current Biology, a Cell Press publication.
"This means that the brain has more extensive systems to make individuals want to overconsume rewards than previously thought," said Alexandra DiFeliceantonio of the University of Michigan, Ann Arbor. "It may be one reason why overconsumption is a problem today."
DiFeliceantonio’s team made the discovery by giving rats an artificial boost with a drug delivered straight to a brain region called the neostriatum. Those animals gorged themselves on more than twice the number of M&M chocolates than they would otherwise have eaten. The researchers also found that enkephalin, the natural drug-like chemical produced in that same brain region, surged when rats began to eat the candy-coated morsels, too.
It’s not that enkephalins or similar drugs make the rats like the chocolates more, the researchers say, but rather that the brain chemicals increase their desire and impulse to eat them.
The findings reveal a surprising extension of the neostriatum’s role, as DiFeliceantonio notes that the brain region had primarily been linked to movement. And there is reason to expect that the findings in rats can tell us a lot about our own binge-eating tendencies.
"The same brain area we tested here is active when obese people see foods and when drug addicts see drug scenes," she says. "It seems likely that our enkephalin findings in rats mean that this neurotransmitter may drive some forms of overconsumption and addiction in people."
The researchers now hope to unravel a related phenomenon that some of us might wish we could do more to control: what happens in our brains when we pass by our favorite fast food restaurant and feel that sudden desire to stop.
Fear can be erased from the brain
Newly formed emotional memories can be erased from the human brain. This is shown by researchers from Uppsala University in a new study now being published by the academic journal Science. The findings may represent a breakthrough in research on memory and fear. Thomas Ågren, a doctoral candidate at the Department of Psychology under the supervision of Professors Mats Fredrikson and Tomas Furmark, has shown, that it is possible to erase newly formed emotional memories from the human brain.
When a person learns something, a lasting long-term memory is created with the aid of a process of consolidation, which is based on the formation of proteins. When we remember something, the memory becomes unstable for a while and is then restabilized by another consolidation process. In other words, it can be said that we are not remembering what originally happened, but rather what we remembered the last time we thought about what happened. By disrupting the reconsolidation process that follows upon remembering, we can affect the content of memory.
Dyslexia Impairs Speech Recognition but Can Spare Phonological Competence
Dyslexia is associated with numerous deficits to speech processing. Accordingly, a large literature asserts that dyslexics manifest a phonological deficit. Few studies, however, have assessed the phonological grammar of dyslexics, and none has distinguished a phonological deficit from a phonetic impairment. Here, we show that these two sources can be dissociated. Three experiments demonstrate that a group of adult dyslexics studied here is impaired in phonetic discrimination (e.g., ba vs. pa), and their deficit compromises even the basic ability to identify acoustic stimuli as human speech. Remarkably, the ability of these individuals to generalize grammatical phonological rules is intact. Like typical readers, these Hebrew-speaking dyslexics identified ill-formed AAB stems (e.g., titug) as less wordlike than well-formed ABB controls (e.g., gitut), and both groups automatically extended this rule to nonspeech stimuli, irrespective of reading ability. The contrast between the phonetic and phonological capacities of these individuals demonstrates that the algebraic engine that generates phonological patterns is distinct from the phonetic interface that implements them. While dyslexia compromises the phonetic system, certain core aspects of the phonological grammar can be spared.