Posts tagged neuroscience

ScienceDaily (Mar. 13, 2012) — People often wonder if computers make children smarter. Scientists at the University of California, Berkeley, are asking the reverse question: Can children make computers smarter? And the answer appears to be ‘yes.’

Research indicates that babies and toddlers do most of their learning as they “play.” (Credit: © matka_Wariatka / Fotolia)

UC Berkeley researchers are tapping the cognitive smarts of babies, toddlers and preschoolers to program computers to think more like humans.

If replicated in machines, the computational models based on baby brainpower could give a major boost to artificial intelligence, which historically has had difficulty handling nuances and uncertainty, researchers said

"Children are the greatest learning machines in the universe. Imagine if computers could learn as much and as quickly as they do," said Alison Gopnik a developmental psychologist at UC Berkeley and author of "The Scientist in the Crib" and "The Philosophical Baby."

In a wide range of experiments involving lollipops, flashing and spinning toys, and music makers, among other props, UC Berkeley researchers are finding that children — at younger and younger ages — are testing hypotheses, detecting statistical patterns and drawing conclusions while constantly adapting to changes.

"Young children are capable of solving problems that still pose a challenge for computers, such as learning languages and figuring out causal relationships," said Tom Griffiths, director of UC Berkeley’s Computational Cognitive Science Lab. "We are hoping to make computers smarter by making them a little more like children."

For example, researchers said, computers programmed with kids’ cognitive smarts could interact more intelligently and responsively with humans in applications such as computer tutoring programs and phone-answering robots.

And that’s not all.

Read more …

March 12th, 2012

Regular use of cholesterol-lowering statin drugs may be associated with a modest reduction in risk for developing Parkinson disease, particularly among younger patients, according to a study in the March issue of Archives of Neurology, one of the JAMA Archives journals.

Statins are one of the most prescribed classes of drugs in the United States and some researchers have hypothesized that the anti-inflammatory and immunomodulating effects of these medications may be neuroprotective. However, statins also may have unfavorable effects on lowering the level of plasma coenzyme Q10, which may be neuroprotective in patients with Parkinson disease (PD), the researchers write in their study background.

Xiang Gao, M.D., Ph.D., of Brigham and Women’s Hospital and Harvard School of Public Health, Boston, and colleagues conducted a prospective study that included 38,192 men and 90,874 women participating in the Health Professional Follow-up study and the Nurses’ Health study.

During 12 years of follow-up from 1994 to 2006, researchers documented 644 incident PD cases (338 in women and 306 in men).

“In summary, we observed an association between regular use of statins and lower risk of developing PD, particularly among younger patients,” the researchers comment. “However, our results should be interpreted with caution because only approximately 70 percent of users of cholesterol-lowering drugs at baseline were actual statin users. Further, the results were only marginally significant and could be due to chance.”

Researchers note that because they classified the use of any cholesterol-lowering drugs before 2000 as statin use, misclassification was inevitably introduced. They also did not collect information on the use of specific statins, which could have different effects on the central nervous system.

When researchers did observe a significant interaction between statin use and age in relation to PD risk it was among study participants younger than 60 years at the start of follow-up, not among those participants who were older.

The authors note that not only have epidemiologic studies produced mixed results on statin use and PD risk, but statins also may have unfavorable effects on the central nervous system.

“In contrast with use of ibuprofen, which has been consistently found to be inversely associated with PD risk in these cohorts as well as in other longitudinal studies, the overall epidemiological evidence relating stain use to PD risk remains unconvincing,” the authors conclude. “Given the potential adverse effects of statins, further prospective observational studies are needed to explore the potential effects of different subtypes of statin on risk of PD and other neurodegenerative diseases.”
(Arch Neurol. 2012;69[3]:380-384).

Source: Neuroscience News

March 12th, 2012

Scientists from the Monell Center report that seven of 12 related mammalian species have lost the sense of sweet taste. As each of the sweet-blind species eats only meat, the findings demonstrate that a liking for sweets is frequently lost during the evolution of diet specialization.

Previous research from the Monell team had revealed the remarkable finding that both domestic and wild cats are unable to taste sweet compounds due to defects in a gene that controls structure of the sweet taste receptor.

Cats are obligate carnivores, meaning that they subsist only on meat. In the current study, published online in Proceedings of the National Academy of Sciences USA, the Monell scientists next asked whether other strict carnivores have also lost the sweet taste receptor.

To do this, they examined sweet taste receptor genes from 12 related mammalian species with varying dietary habits. They once again found taste loss and to their surprise, it was widespread in the meat-eating species.

Senior author Gary Beauchamp, Ph.D., a behavioral biologist at Monell, comments, “Sweet taste was thought to be nearly a universal trait in animals. That evolution has independently led to its loss in so many different species was quite unexpected.”

Read more …

ScienceDaily (Mar. 8, 2012) — A new study in Science suggests that thrill-seeking is not limited to humans and other vertebrates. Some honey bees, too, are more likely than others to seek adventure. The brains of these novelty-seeking bees exhibit distinct patterns of gene activity in molecular pathways known to be associated with thrill-seeking in humans, researchers report.

A new study in Science suggests that thrill-seeking is not limited to humans and other vertebrates. Some honey bees, too, are more likely than others to seek adventure. (Credit: L. Brian Stauffer)

The findings offer a new window on the inner life of the honey bee hive, which once was viewed as a highly regimented colony of seemingly interchangeable workers taking on a few specific roles (nurse or forager, for example) to serve their queen. Now it appears that individual honey bees actually differ in their desire or willingness to perform particular tasks, said University of Illinois entomology professor and Institute for Genomic Biology director

Read more …

ScienceDaily (Mar. 8, 2012) — How do neurons in the brain communicate with each other? One common theory suggests that individual cells do not exchange signals among each other, but rather that exchange takes place between groups of cells. Researchers from Japan, the United States and Germany have now developed a mathematical model that can be used to test this assumption. Their results have been published in the current issue of the journal “PLoS Computational Biology.”

A neuron in the neocortex, the part of the brain that deals with higher brain functions, contacts thousands of other neurons and receives as many inputs from other neurons. Previously, it has been very difficult to use measured signals to interpret the way the cells work together. Scientists at the RIKEN Brain Science Institute (BSI) in Japan have now joined forces with researchers at the Forschungszentrum Jülich, Germany, and MIT in Boston, USA, to develop a mathematical model that can clarify the way neurons collaborate.

"From the many signals measured in parallel, the novel method filters the information on whether the neurons communicate individually or as a group," explains Dr. Hideaki Shimazaki from BSI. "Furthermore it takes into account that these groups of cells are not fixed but, instead, can organize themselves flexibly within milliseconds into groups of different composition, depending on the current requirements of the brain."

Prof. Sonja Grün from Forschungszentrum Jülich hopes that the method can help researchers to prove the existence of dynamic cell assemblies and clearly assign their activities to certain behaviors. The scientists already demonstrated that neurons work together when an animal anticipates a signal, which may allow it to have a more rapid or more sensitive response.

In future, the scientists hope to learn how to use their methods on the signals recorded from hundreds of neurons simultaneously. This would raise the probability of observing cell assemblies involved in planning and controlling behavior.

Source: Science Daily

ScienceDaily (Mar. 8, 2012) — UT Southwestern Medical Center investigators have identified a genetic manipulation that increases the development of neurons in the brain during aging and enhances the effect of antidepressant drugs.

UT Southwestern Medical Center investigators have identified a genetic manipulation that increases the development of neurons in the brain during aging and enhances the effect of antidepressant drugs. (Credit: © rolffimages / Fotolia)

The research finds that deleting the Nf1 gene in mice results in long-lasting improvements in neurogenesis, which in turn makes those in the test group more sensitive to the effects of antidepressants.

"The significant implication of this work is that enhancing neurogenesis sensitizes mice to antidepressants — meaning they needed lower doses of the drugs to affect ‘mood’ — and also appears to have anti-depressive and anti-anxiety effects of its own that continue over time," said Dr. Luis Parada, director of the Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration and senior author of the study published in The Journal of Neuroscience.

Just as in people, mice produce new neurons throughout adulthood, although the rate declines with age and stress, said Dr. Parada, chairman of developmental biology at UT Southwestern. Studies have shown that learning, exercise, electroconvulsive therapy and some antidepressants can increase neurogenesis. The steps in the process are well known but the cellular mechanisms behind those steps are not.

"In neurogenesis, stem cells in the brain’s hippocampus give rise to neuronal precursor cells that eventually become young neurons, which continue on to become full-fledged neurons that integrate into the brain’s synapses," said Dr. Parada, an elected member of the National Academy of Sciences, its Institute of Medicine, and the American Academy of Arts and Sciences.

The researchers used a sophisticated process to delete the gene that codes for the Nf1 protein only in the brains of mice, while production in other tissues continued normally. After showing that mice lacking Nf1 protein in the brain had greater neurogenesis than controls, the researchers administered behavioral tests designed to mimic situations that would spark a subdued mood or anxiety, such as observing grooming behavior in response to a small splash of sugar water.

The researchers found that the test group mice formed more neurons over time compared to controls, and that young mice lacking the Nf1 protein required much lower amounts of anti-depressants to counteract the effects of stress. Behavioral differences between the groups persisted at three months, six months and nine months. “Older mice lacking the protein responded as if they had been taking antidepressants all their lives,” said Dr. Parada.

"In summary, this work suggests that activating neural precursor cells could directly improve depression- and anxiety-like behaviors, and it provides a proof-of-principle regarding the feasibility of regulating behavior via direct manipulation of adult neurogenesis," Dr. Parada said.

Dr. Parada’s laboratory has published a series of studies that link the Nf1 gene — best known for mutations that cause tumors to grow around nerves — to wide-ranging effects in several major tissues. For instance, in one study researchers identified ways that the body’s immune system promotes the growth of tumors, and in another study, they described how loss of the Nf1 protein in the circulatory system leads to hypertension and congenital heart disease.

Source: Science Daily

March 9, 2012

(Medical Xpress) — Despite a century of research, memory encoding in the brain has remained mysterious. Neuronal synaptic connection strengths are involved, but synaptic components are short-lived while memories last lifetimes. This suggests synaptic information is encoded and hard-wired at a deeper, finer-grained molecular scale.

In an article in the March 8 issue of the journal PLoS Computational Biology, physicists Travis Craddock and Jack Tuszynski of the University of Alberta, and anesthesiologist Stuart Hameroff of the University of Arizona demonstrate a plausible mechanism for encoding synaptic memory in microtubules, major components of the structural cytoskeleton within neurons.

Microtubules are cylindrical hexagonal lattice polymers of the protein tubulin, comprising 15 percent of total brain protein. Microtubules define neuronal architecture, regulate synapses, and are suggested to process information via interactive bit-like states of tubulin. But any semblance of a common code connecting microtubules to synaptic activity has been missing. Until now.

The standard experimental model for neuronal memory is long term potentiation (LTP) in which brief pre-synaptic excitation results in prolonged post-synaptic sensitivity. An essential player in LTP is the hexagonal enzyme calcium/calmodulin-dependent protein kinase II (CaMKII). Upon pre-synaptic excitation, calcium ions entering post-synaptic neurons cause the snowflake-shaped CaMKII to transform, extending sets of 6 leg-like kinase domains above and below a central domain, the activated CaMKII resembling a double-sided insect. Each kinase domain can phosphorylate a substrate, and thus encode one bit of synaptic information. Ordered arrays of bits are termed bytes, and 6 kinase domains on one side of each CaMKII can thus phosphorylate and encode calcium-mediated synaptic inputs as 6-bit bytes. But where is the intra-neuronal substrate for memory encoding by CaMKII phosphorylation? Enter microtubules.

Using molecular modeling, Craddock et al reveal a perfect match among spatial dimensions, geometry and electrostatic binding of the insect-like CaMKII, and hexagonal lattices of tubulin proteins in microtubules. They show how CaMKII kinase domains can collectively bind and phosphorylate 6-bit bytes, resulting in hexagonally-based patterns of phosphorylated tubulins in microtubules. Craddock et al calculate enormous information capacity at low energy cost, demonstrate microtubule-associated protein logic gates, and show how patterns of phosphorylated tubulins in microtubules can control neuronal functions by triggering axonal firings, regulating synapses, and traversing scale.

Microtubules and CaMKII are ubiquitous in eukaryotic biology, extremely rich in brain neurons, and capable of connecting membrane and cytoskeletal levels of information processing. Decoding and stimulating microtubules could enable therapeutic intervention in a host of pathological processes, for example Alzheimer’s disease in which microtubule disruption plays a key role, and brain injury in which microtubule activities can repair neurons and synapses.

Hameroff, senior author on the study, said: “Many neuroscience papers conclude by claiming their findings may help understand how the brain works, and treat Alzheimer’s, brain injury and various neurological and psychiatric disorders. This study may actually do that. We may have a glimpse of the brain’s biomolecular code for memory.”

Provided by University of Arizona

Source: medicalxpress.com

ScienceDaily (Mar. 8, 2012) — The hair cells of the inner ear have a previously unknown “root” extension that may allow them to communicate with nerve cells and the brain to regulate sensitivity to sound vibrations and head position, researchers at the University of Illinois at Chicago College of Medicine have discovered.

Type 2 hair cell with hair cell rootlets ending as expected in the cuticular plate. (Credit: Copyright University of Illinois Board of Trustees/Artist, Anna Lysakowski)

Their finding is reported online in advance of print in the Proceedings of the National Academy of Sciences.

The hair-like structures, called stereocilia, are fairly rigid and are interlinked at their tops by structures called tip-links.

When you move your head, or when a sound vibration enters your ear, motion of fluid in the ear causes the tip-links to get displaced and stretched, opening up ion channels and exciting the cell, which can then relay information to the brain, says Anna Lysakowski, professor of anatomy and cell biology at the UIC College of Medicine and principal investigator on the study.

Read more …

ScienceDaily (Mar. 8, 2012) — In both animals and humans, vocal signals used for communication contain a wide array of different sounds that are determined by the vibrational frequencies of vocal cords. For example, the pitch of someone’s voice, and how it changes as they are speaking, depends on a complex series of varying frequencies. Knowing how the brain sorts out these different frequencies — which are called frequency-modulated (FM) sweeps — is believed to be essential to understanding many hearing-related behaviors, like speech. Now, a pair of biologists at the California Institute of Technology (Caltech) has identified how and where the brain processes this type of sound signal.

This diagram shows areas in the midbrain region where direction- selective neurons were found. (Credit: Guangying Wu/Caltech)

Their findings are outlined in a paper published in the March 8 issue of the journal Neuron.

Read more …