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neurosciencestuff:

Try, try again? Study says no

When it comes to learning languages, adults and children have different strengths. Adults excel at absorbing the vocabulary needed to navigate a grocery store or order food in a restaurant, but children have an uncanny ability to pick up on subtle nuances of language that often elude adults. Within months of living in a foreign country, a young child may speak a second language like a native speaker.

Brain structure plays an important role in this “sensitive period” for learning language, which is believed to end around adolescence. The young brain is equipped with neural circuits that can analyze sounds and build a coherent set of rules for constructing words and sentences out of those sounds. Once these language structures are established, it’s difficult to build another one for a new language.

In a new study, a team of neuroscientists and psychologists led by Amy Finn, a postdoc at MIT’s McGovern Institute for Brain Research, has found evidence for another factor that contributes to adults’ language difficulties: When learning certain elements of language, adults’ more highly developed cognitive skills actually get in the way. The researchers discovered that the harder adults tried to learn an artificial language, the worse they were at deciphering the language’s morphology — the structure and deployment of linguistic units such as root words, suffixes, and prefixes.

“We found that effort helps you in most situations, for things like figuring out what the units of language that you need to know are, and basic ordering of elements. But when trying to learn morphology, at least in this artificial language we created, it’s actually worse when you try,” Finn says.

Finn and colleagues from the University of California at Santa Barbara, Stanford University, and the University of British Columbia describe their findings in the July 21 issue of PLoS One. Carla Hudson Kam, an associate professor of linguistics at British Columbia, is the paper’s senior author.

Too much brainpower

Linguists have known for decades that children are skilled at absorbing certain tricky elements of language, such as irregular past participles (examples of which, in English, include “gone” and “been”) or complicated verb tenses like the subjunctive.

“Children will ultimately perform better than adults in terms of their command of the grammar and the structural components of language — some of the more idiosyncratic, difficult-to-articulate aspects of language that even most native speakers don’t have conscious awareness of,” Finn says.

In 1990, linguist Elissa Newport hypothesized that adults have trouble learning those nuances because they try to analyze too much information at once. Adults have a much more highly developed prefrontal cortex than children, and they tend to throw all of that brainpower at learning a second language. This high-powered processing may actually interfere with certain elements of learning language.

“It’s an idea that’s been around for a long time, but there hasn’t been any data that experimentally show that it’s true,” Finn says.

Finn and her colleagues designed an experiment to test whether exerting more effort would help or hinder success. First, they created nine nonsense words, each with two syllables. Each word fell into one of three categories (A, B, and C), defined by the order of consonant and vowel sounds.

Study subjects listened to the artificial language for about 10 minutes. One group of subjects was told not to overanalyze what they heard, but not to tune it out either. To help them not overthink the language, they were given the option of completing a puzzle or coloring while they listened. The other group was told to try to identify the words they were hearing.

Each group heard the same recording, which was a series of three-word sequences — first a word from category A, then one from category B, then category C — with no pauses between words. Previous studies have shown that adults, babies, and even monkeys can parse this kind of information into word units, a task known as word segmentation.

Subjects from both groups were successful at word segmentation, although the group that tried harder performed a little better. Both groups also performed well in a task called word ordering, which required subjects to choose between a correct word sequence (ABC) and an incorrect sequence (such as ACB) of words they had previously heard.

The final test measured skill in identifying the language’s morphology. The researchers played a three-word sequence that included a word the subjects had not heard before, but which fit into one of the three categories. When asked to judge whether this new word was in the correct location, the subjects who had been asked to pay closer attention to the original word stream performed much worse than those who had listened more passively.

“This research is exciting because it provides evidence indicating that effortful learning leads to different results depending upon the kind of information learners are trying to master,” says Michael Ramscar, a professor of linguistics at the University of Tübingen who was not part of the research team. “The results indicate that learning to identify relatively simple parts of language, such as words, is facilitated by effortful learning, whereas learning more complex aspects of language, such as grammatical features, is impeded by effortful learning.”

Turning off effort

The findings support a theory of language acquisition that suggests that some parts of language are learned through procedural memory, while others are learned through declarative memory. Under this theory, declarative memory, which stores knowledge and facts, would be more useful for learning vocabulary and certain rules of grammar. Procedural memory, which guides tasks we perform without conscious awareness of how we learned them, would be more useful for learning subtle rules related to language morphology.

“It’s likely to be the procedural memory system that’s really important for learning these difficult morphological aspects of language. In fact, when you use the declarative memory system, it doesn’t help you, it harms you,” Finn says.

Still unresolved is the question of whether adults can overcome this language-learning obstacle. Finn says she does not have a good answer yet but she is now testing the effects of “turning off” the adult prefrontal cortex using a technique called transcranial magnetic stimulation. Other interventions she plans to study include distracting the prefrontal cortex by forcing it to perform other tasks while language is heard, and treating subjects with drugs that impair activity in that brain region.

neurosciencestuff:

Blame it on the astrocytes

In the brains of all vertebrates, information is transmitted through synapses, a mechanism that allows an electric or chemical signal to be passed from one brain cell to another. Chemical synapses, which are the most abundant type of synapse, can be either excitatory or inhibitory. Synapse formation is crucial for learning, memory, perception and cognition, and the balance between excitatory and inhibitory synapses critical for brain function. For instance, every time we learn something, the new information is transformed into memory through synaptic plasticity, a process in which synapses are strengthened and become more responsive to different stimuli or environmental cues. Synapses may change their shape or function in a matter of seconds or over an entire lifetime. In humans, a number of disorders are associated with dysfunctional synapses, including autism, epilepsy, substance abuse and depression.

Astrocytes, named for their star-like shape, are ubiquitous brain cells known for regulating excitatory synapse formation through cells. Recent studies have shown that astrocytes also play a role in forming inhibitory synapses, but the key players and underlying mechanisms have remained unknown until now.

A new study just published in the journal Glia and available online on July 11th, details the newly discovered mechanism by which astrocytes are involved in inhibitory synapse formation and presents strong evidence that Transforming Growth Factor Beta 1 (TGF β1), a protein produced by many cell types (including astrocytes) is a key player in this process. The team led by Flávia Gomes of the Rio de Janeiro Institute of Biomedical Sciences at the Federal University of Rio de Janeiro investigated the process in both mouse and human tissues, first in test tubes, then in living brain cells.

Previous evidence has shown that TGF β1, a molecule associated with essential functions in nervous system development and repair, modulates other components responsible for normal brain function. In this study, the authors were able to show that TGF β1 triggers N-methyl-D-aspartate receptor (NMDA), a molecule controlling memory formation and maintenance through synaptic plasticity. In the study, the group also shows that TGF β1-induction of inhibitory synapses depends on activation of another molecule - Ca2+/calmodulin-dependent protein kinase II (CaMK2)-, which works as a mediator for learning and memory. “Our study is the first to associate this complex pathway of molecules, of which TGF β1 seems to be a key player, to astrocytes’ ability to modulate inhibitory synapses”, says Flávia Gomes.

The idea that the balance between excitatory and inhibitory inputs depends on astrocyte signals gains strong support with this new study and suggests a pivotal role for astrocytes in the development of neurological disorders involving impaired inhibitory synapse transmission. Knowing the players and mechanisms underlying inhibitory synapses may improve our understanding of synaptic plasticity and cognitive processes and may help develop new drugs for treating these diseases.

(Image credit)

neurosciencestuff:

Restoring Active Memory Program Poised to Launch

Teams will develop and test implantable therapeutic devices for memory restoration in patients with memory deficits caused by disease or trauma

DARPA has selected two universities to initially lead the agency’s Restoring Active Memory (RAM) program, which aims to develop and test wireless, implantable “neuroprosthetics” that can help servicemembers, veterans, and others overcome memory deficits incurred as a result of traumatic brain injury (TBI) or disease.

The University of California, Los Angeles (UCLA), and the University of Pennsylvania (Penn) will each head a multidisciplinary team to develop and test electronic interfaces that can sense memory deficits caused by injury and attempt to restore normal function. Under the terms of separate cooperative agreements with DARPA, UCLA will receive up to $15 million and Penn will receive up to $22.5 million over four years, with full funding contingent on the performer teams successfully meeting a series of technical milestones. DARPA also has a cooperative agreement worth up to $2.5 million in place with Lawrence Livermore National Laboratory to develop an implantable neural device for the UCLA-led effort.

“The start of the Restoring Active Memory program marks an exciting opportunity to reveal many new aspects of human memory and learn about the brain in ways that were never before possible,” said DARPA Program Manager Justin Sanchez. “Anyone who has witnessed the effects of memory loss in another person knows its toll and how few options are available to treat it. We’re going to apply the knowledge and understanding gained in RAM to develop new options for treatment through technology.”

TBI is a serious cause of disability in the United States. Diagnosed in more than 270,000 military servicemembers since 2000 and affecting an estimated 1.7 million U.S. civilians each year, TBI frequently results in an impaired ability to retrieve memories formed prior to injury and a reduced capacity to form or retain new memories following injury. Despite the scale of the problem, no effective therapies currently exist to mitigate the long-term consequences of TBI on memory. Through the RAM program, DARPA seeks to accelerate the development of technology needed to address this public health challenge and help servicemembers and others overcome memory deficits by developing new neuroprosthetics to bridge gaps in the injured brain.

“We owe it to our service members to accelerate research that can minimize the long-term impacts of their injuries,” Sanchez said. “Despite increasingly aggressive prevention efforts, traumatic brain injury remains a serious problem in military and civilian sectors. Through the Restoring Active Memory program, DARPA aims to better understand the underlying neurological basis of memory loss and speed the development of innovative therapies.”

Specifically, RAM performers aim to develop and test wireless, fully implantable neural-interface medical devices that can serve as “neuroprosthetics”—technology that can effectively bridge the gaps that interfere with an individual’s ability to encode new memories or retrieve old ones.

To start, DARPA will support the development of multi-scale computational models with high spatial and temporal resolution that describe how neurons code declarative memories—those well-defined parcels of knowledge that can be consciously recalled and described in words, such as events, times, and places. Researchers will also explore new methods for analysis and decoding of neural signals to understand how targeted stimulation might be applied to help the brain reestablish an ability to encode new memories following brain injury. “Encoding” refers to the process by which newly learned information is attended to and processed by the brain when first encountered.

Building on this foundational work, researchers will attempt to integrate the computational models developed under RAM into new, implantable, closed-loop systems able to deliver targeted neural stimulation that may ultimately help restore memory function. These studies will involve volunteers living with deficits in the encoding and/or retrieval of declarative memories and/or volunteers undergoing neurosurgery for other neurological conditions.

Unique to the UCLA team’s approach is a focus on the portion of the brain known as the entorhinal area. UCLA researchers previously demonstrated that human memory could be facilitated by stimulating that region, which is known to be involved in learning and memory. Considered the entrance to the hippocampus—which helps form and store memories—the entorhinal area plays a crucial role in transforming daily experience into lasting memories. Data collected during the first year of the project from patients already implanted with brain electrodes as part of their treatment for epilepsy will be used to develop a computational model of the hippocampal-entorhinal system that can then be used to test memory restoration in patients.

After developing an advanced, new wireless neuromodulation device—featuring ten-times smaller size and much higher spatial resolution than existing devices—the UCLA team will implant such devices into the entorhinal area and hippocampus of patients with traumatic brain injury.

The Penn team’s approach is based on an understanding that memory is the result of complex interactions among widespread brain regions. Researchers will study neurosurgical patients who have electrodes implanted in multiple areas of their brains for the treatment of various neurological conditions. By recording neural activity from these electrodes as patients play computer-based memory games, the researchers will measure “biomarkers” of successful memory function—patterns of activity that accompany the successful formation of new memories and the successful retrieval of old ones. Researchers could then use those models and a novel neural stimulation and monitoring system—being developed in partnership with Medtronic—to restore brain memory function. The investigational system will simultaneously monitor and stimulate a number of brain sites, which may lead to better understandings of the brain and how brain stimulation therapy can potentially restore normal brain function following injury or the onset of neuropsychological illness.

In addition to human clinical efforts, RAM will support animal studies to advance the state-of-the-art of quantitative models that account for the encoding and retrieval of complex memories and memory attributes, including their hierarchical associations with one another. This work will also seek to identify any characteristic neural and behavioral correlates of memories facilitated by therapeutic devices.

totallyfubar:

I have a physics textbook from before the electron was discovered and they just sound so frustrated it’s hilarious

(via tegoshiyuya)

neurosciencestuff:

Sleep deprivation leads to symptoms of schizophrenia
Psychologists at the University of Bonn are amazed by the severe deficits caused by a sleepless night
Twenty-four hours of sleep deprivation can lead to conditions in healthy persons similar to the symptoms of schizophrenia. This discovery was made by an international team of researchers under the guidance of the University of Bonn and King’s College London. The scientists point out that this effect should be investigated more closely in persons who have to work at night. In addition, sleep deprivation may serve as a model system for the development of drugs to treat psychosis. The results have now been published in “The Journal of Neuroscience”.
In psychosis, there is a loss of contact with reality and this is associated with hallucinations and delusions. The chronic form is referred to as schizophrenia, which likewise involves thought disorders and misperceptions. Affected persons report that they hear voices, for example. Psychoses rank among the most severe mental illnesses. An international team of researchers under the guidance of the University of Bonn has now found out that after 24 hours of sleep deprivation in healthy patients, numerous symptoms were noted which are otherwise typically attributed to psychosis or schizophrenia. “It was clear to us that a sleepless night leads to impairment in the ability to concentrate,” says Prof. Dr. Ulrich Ettinger of the Cognitive Psychology Unit in the Department of Psychology at the University of Bonn. “But we were surprised at how pronounced and how wide the spectrum of schizophrenia-like symptoms was.”
The scientists from the University of Bonn, King’s College London (England) as well as the Department of Psychiatry and Psychotherapy of the University of Bonn Hospital examined a total of 24 healthy subjects of both genders aged 18 to 40 in the sleep laboratory of the Department of Psychology. In an initial run, the test subjects were to sleep normally in the laboratory. About one week later, they were kept awake all night with movies, conversation, games and brief walks. On the following morning, subjects were each asked about their thoughts and feelings. In addition, subjects underwent a measurement known as prepulse inhibition.
Unselected information leads to chaos in the brain
"Prepulse inhibition is a standard test to measure the filtering function of the brain,” explains lead author Dr. Nadine Petrovsky from Prof. Ettinger’s team. In the experiment, a loud noise is heard via headphones. As a result, the test subjects experience a startle response, which is recorded with electrodes through the contraction of facial muscles. If a weaker stimulus is emitted beforehand as a “prepulse”, the startle response is lower. “The prepulse inhibition demonstrates an important function of the brain: Filters separate what is important from what is not important and prevent sensory overload,” says Dr. Petrovsky.
In our subjects, this filtering function of the brain was significantly reduced following a sleepless night. “There were pronounced attention deficits, such as what typically occurs in the case of schizophrenia,” reports Prof. Ettinger. “The unselected flood of information led to chaos in the brain.” Following sleep deprivation, the subjects also indicated in questionnaires that they were somewhat more sensitive to light, color or brightness. Accordingly, their sense of time and sense of smell were altered and mental leaps were reported. Many of those who spent the night even had the impression of being able to read thoughts or notice altered body perception. “We did not expect that the symptoms could be so pronounced after one night spent awake,” says the psychologist from the University of Bonn.
Sleep deprivation as a model system for mental illnesses
The scientists see an important potential application for their results in research for drugs to treat psychoses. “In drug development, mental disorders like these have been simulated to date in experiments using certain active substances. However, these convey the symptoms of psychoses in only a very limited manner,” says Prof. Ettinger. Sleep deprivation may be a much better model system because the subjective symptoms and the objectively measured filter disorder are far more akin to mental illnesses. Of course, the sleep deprivation model is not harmful: After a good night’s recovery sleep, the symptoms disappear. There is also a need for research with regard to persons who regularly have to work at night. “Whether the symptoms of sleep deprivation gradually become weaker due to acclimatization has yet to be investigated,” says the psychologist from the University of Bonn.
(Image: Getty)

neurosciencestuff:

Sleep deprivation leads to symptoms of schizophrenia

Psychologists at the University of Bonn are amazed by the severe deficits caused by a sleepless night

Twenty-four hours of sleep deprivation can lead to conditions in healthy persons similar to the symptoms of schizophrenia. This discovery was made by an international team of researchers under the guidance of the University of Bonn and King’s College London. The scientists point out that this effect should be investigated more closely in persons who have to work at night. In addition, sleep deprivation may serve as a model system for the development of drugs to treat psychosis. The results have now been published in “The Journal of Neuroscience”.

In psychosis, there is a loss of contact with reality and this is associated with hallucinations and delusions. The chronic form is referred to as schizophrenia, which likewise involves thought disorders and misperceptions. Affected persons report that they hear voices, for example. Psychoses rank among the most severe mental illnesses. An international team of researchers under the guidance of the University of Bonn has now found out that after 24 hours of sleep deprivation in healthy patients, numerous symptoms were noted which are otherwise typically attributed to psychosis or schizophrenia. “It was clear to us that a sleepless night leads to impairment in the ability to concentrate,” says Prof. Dr. Ulrich Ettinger of the Cognitive Psychology Unit in the Department of Psychology at the University of Bonn. “But we were surprised at how pronounced and how wide the spectrum of schizophrenia-like symptoms was.”

The scientists from the University of Bonn, King’s College London (England) as well as the Department of Psychiatry and Psychotherapy of the University of Bonn Hospital examined a total of 24 healthy subjects of both genders aged 18 to 40 in the sleep laboratory of the Department of Psychology. In an initial run, the test subjects were to sleep normally in the laboratory. About one week later, they were kept awake all night with movies, conversation, games and brief walks. On the following morning, subjects were each asked about their thoughts and feelings. In addition, subjects underwent a measurement known as prepulse inhibition.

Unselected information leads to chaos in the brain

"Prepulse inhibition is a standard test to measure the filtering function of the brain,” explains lead author Dr. Nadine Petrovsky from Prof. Ettinger’s team. In the experiment, a loud noise is heard via headphones. As a result, the test subjects experience a startle response, which is recorded with electrodes through the contraction of facial muscles. If a weaker stimulus is emitted beforehand as a “prepulse”, the startle response is lower. “The prepulse inhibition demonstrates an important function of the brain: Filters separate what is important from what is not important and prevent sensory overload,” says Dr. Petrovsky.

In our subjects, this filtering function of the brain was significantly reduced following a sleepless night. “There were pronounced attention deficits, such as what typically occurs in the case of schizophrenia,” reports Prof. Ettinger. “The unselected flood of information led to chaos in the brain.” Following sleep deprivation, the subjects also indicated in questionnaires that they were somewhat more sensitive to light, color or brightness. Accordingly, their sense of time and sense of smell were altered and mental leaps were reported. Many of those who spent the night even had the impression of being able to read thoughts or notice altered body perception. “We did not expect that the symptoms could be so pronounced after one night spent awake,” says the psychologist from the University of Bonn.

Sleep deprivation as a model system for mental illnesses

The scientists see an important potential application for their results in research for drugs to treat psychoses. “In drug development, mental disorders like these have been simulated to date in experiments using certain active substances. However, these convey the symptoms of psychoses in only a very limited manner,” says Prof. Ettinger. Sleep deprivation may be a much better model system because the subjective symptoms and the objectively measured filter disorder are far more akin to mental illnesses. Of course, the sleep deprivation model is not harmful: After a good night’s recovery sleep, the symptoms disappear. There is also a need for research with regard to persons who regularly have to work at night. “Whether the symptoms of sleep deprivation gradually become weaker due to acclimatization has yet to be investigated,” says the psychologist from the University of Bonn.

(Image: Getty)

neurosciencestuff:

Neuroscientists study our love for deep bass sounds

Have you ever wondered why bass-range instruments tend to lay down musical rhythms, while instruments with a higher pitch often handle the melody?

According to new research from Laurel Trainor and colleagues at the McMaster Institute for Music and The Mind, this is no accident, but rather a result of the physiology of hearing.

In other words, when the bass is loud and rock solid, we have an easier time following along to the rhythm of a song.

Read more

neurosciencestuff:

Tool helps guide brain cancer surgery

A tool to help brain surgeons test and more precisely remove cancerous tissue was successfully used during surgery, according to a Purdue University and Brigham and Women’s Hospital study.

The Purdue-designed tool sprays a microscopic stream of charged solvent onto the tissue surface to gather information about its molecular makeup and produces a color-coded image that reveals the location, nature and concentration of tumor cells.

 ”In a matter of seconds this technique offers molecular information that can detect residual tumor that otherwise may have been left behind in the patient,” said R. Graham Cooks, the Purdue professor who co-led the research team. “The instrumentation is relatively small and inexpensive and could easily be installed in operating rooms to aid neurosurgeons. This study shows the tremendous potential it has to enhance patient care.”

Current surgical methods rely on the surgeon’s trained eye with the help of an operating microscope and imaging from scans performed before surgery, Cooks said.

"Brain tumor tissue looks very similar to healthy brain tissue, and it is very difficult to determine where the tumor ends and the normal tissue begins," he said. "In the brain, millimeters of tissue can mean the difference between normal and impaired function. Molecular information beyond what a surgeon can see can help them precisely and comprehensively remove the cancer."

The mass spectrometry-based tool had previously been shown to accurately identify the cancer type, grade and tumor margins of specimens removed during surgery based on an evaluation of the distribution and amounts of fatty substances called lipids within the tissue. This study took the analysis a step further by additionally evaluating a molecule associated with cell growth and differentiation that is considered a biomarker for certain types of brain cancer, he said.

"We were able to identify a single metabolite biomarker that provides information about tumor classification, genotype and the prognosis for the patient," said Cooks, the Henry Bohn Hass Distinguished Professor of Chemistry. "Through mass spectrometry all of this information can be obtained from a biopsy in a matter of minutes and without significantly interrupting the surgical procedure."

For this study, which included validation on samples and use during two patients’ surgical procedures, the tool was tuned to identify the lipid metabolite 2-hydroxyglutarate or 2-HG. This biomarker is associated with more than 70 percent of gliomas and can be used to classify the tumors, he said.  

A paper detailing the results of the National Institutes of Health-funded study will be published in an upcoming issue of the Proceedings of the National Academy of Sciences and is published online.

In mass spectrometry molecules are electrically charged and turned into ions so that they can be identified by their mass. The new tool relies an ambient mass spectrometry analysis technique developed by Cooks and his colleagues called desorption electrospray ionization, or DESI, which eliminated the need for chemical manipulations of samples and containment in a vacuum chamber for ionization. DESI allows ionization to occur directly on surfaces outside of the mass spectrometers, making the process much simpler, faster and more applicable to surgical settings.

The tool couples a DESI mass spectrometer with a software program designed by the research team that uses the results to characterize the brain tumors and detect boundaries between healthy and cancerous tissue.  The program is based on earlier studies of lipid patterns that correspond to different types and grades of cancer and currently covers the two most common types of brain tumors, gliomas and meningiomas. These two types of tumors combined account for about 65 percent of all brain tumors and 80 percent of all malignant brain tumors, according to the American Brain Tumor Association.

Additional classification methodologies and metabolite biomarkers could be added to tailor the tool to different types of cancer, Cooks said.

The brain surgery was performed in the Advanced Multi-Modality Image Guided Operating suite, or AMIGO at Brigham and Women’s Hospital.

Dr. Nathalie Agar, director of the Surgical Molecular Imaging Laboratory within the neurosurgery department at Brigham and Women’s Hospital, led the study.

neurosciencestuff:

Study shows moving together builds bonds from the time we learn to walk

Whether they march in unison, row in the same boat or dance to the same song, people who move in time with one another are more likely to bond and work together afterward.

It’s a principle established by previous studies, but now researchers at McMaster have shown that moving in time with others even affects the social behaviour of babies who have barely learned to walk.

“Moving in sync with others is an important part of musical activities,” says Laura Cirelli, lead author of a paper now posted online and scheduled to appear in an upcoming issue of the journal Developmental Science. “These effects show that movement is a fundamental part of music that affects social behavior from a very young age.”

Cirelli and her colleagues in the Department of Psychology, Neuroscience & Behaviour showed that 14-month-old babies were much more likely to help another person after the experience of bouncing up and down in time to music with that person.

Cirelli and fellow doctoral student Kate Einarson worked under the supervision of Professor Laurel Trainor, a specialist in child development research.

They tested 68 babies in all, to see if bouncing to music with another person makes a baby more likely to assist that person by handing back “accidentally” dropped objects.

Working in pairs, one researcher held a baby in a forward-facing carrier and stood facing the second researcher. When the music started to play, both researchers would gently bounce up and down, one bouncing the baby with them. Some babies were bounced in sync with the researcher across from them, and others were bounced at a different tempo.

When the song was over, the researcher who had been facing the baby then performed several simple tasks, including drawing a picture with a marker. While drawing the picture, she would pretend to drop the marker to see whether the infant would pick it up and hand it back to her – a classic test of altruism in babies.

The babies who had been bounced in time with the researcher were much more likely to toddle over, pick up the object and pass it back to the researcher, compared to infants who had been bounced at a different tempo than the experimenter.

While babies who had been bounced out of sync with the researcher only picked up and handed back 30 per cent of the dropped objects, in-sync babies came to the researcher’s aid 50 per cent of the time. The in-sync babies also responded more quickly.

The findings suggest that when we sing, clap, bounce or dance in time to music with our babies, these shared experiences of synchronous movement help form social bonds between us and our babies.

It’s a significant finding, Cirelli believes, because it shows that moving together to music with others encourages the development of altruistic helping behaviour among those in a social group. It suggests that music is an important part of day care and kindergarten curriculums because it helps to build a co-operative social climate.

Cirelli is now researching whether the experience of synchronous movement with one person leads babies to extend their increased helpfulness to other people or whether infants reserve their altruistic behaviour for their dancing partners.

For Science!
Quiz description:
"Which English?

Is Throw me down the stairs my shoes a good English sentence?
The answer depends on where you live. Many people in Newfoundland find that sentence perfectly grammatical.
By taking this quiz, you will be helping train a machine algorithm that is mapping out the differences in English grammar around the world, both in traditionally English-speaking countries and also in countries like Mexico, China, and India.
At the end, you can see our algorithm’s best guess as to which English you speak as well as whether your first (native) language is English or something else.”
Take this quiz here! Other quizzes are also available.

For Science!

Quiz description:

"Which English?

Is Throw me down the stairs my shoes a good English sentence?

The answer depends on where you live. Many people in Newfoundland find that sentence perfectly grammatical.

By taking this quiz, you will be helping train a machine algorithm that is mapping out the differences in English grammar around the world, both in traditionally English-speaking countries and also in countries like Mexico, China, and India.

At the end, you can see our algorithm’s best guess as to which English you speak as well as whether your first (native) language is English or something else.”

Take this quiz here! Other quizzes are also available.

neuromorphogenesis:

Neuroscience’s New Toolbox

With the invention of optogenetics and other technologies, researchers can investigate the source of emotions, memory, and consciousness for the first time.

What might be called the “make love, not war” branch of behavioral neuroscience began to take shape in (where else?) California several years ago, when researchers in David J. Anderson’s laboratory at Caltech decided to tackle the biology of aggression. They initiated the line of research by orchestrating the murine version of Fight Night: they goaded male mice into tangling with rival males and then, with painstaking molecular detective work, zeroed in on a smattering of cells in the hypothalamus that became active when the mice started to fight.

The hypothalamus is a small structure deep in the brain that, among other functions, coördinates sensory inputs—the appearance of a rival, for example—with instinctual behavioral responses. Back in the 1920s, Walter Hess of the University of Zurich (who would win a Nobel in 1949) had shown that if you stuck an electrode into the brain of a cat and electrically stimulated certain regions of the hypothalamus, you could turn a purring feline into a furry blur of aggression. Several interesting hypotheses tried to explain how and why that happened, but there was no way to test them. Like a lot of fundamental questions in brain science, the mystery of aggression didn’t go away over the past century—it just hit the usual empirical roadblocks. We had good questions but no technology to get at the answers.

By 2010, Anderson’s Caltech lab had begun to tease apart the underlying mechanisms and neural circuitry of aggression in their pugnacious mice. Armed with a series of new technologies that allowed them to focus on individual clumps of cells within brain regions, they stumbled onto a surprising anatomical discovery: the tiny part of the hypothalamus that seemed correlated with aggressive behavior was intertwined with the part associated with the impulse to mate. That small duchy of cells—the technical name is the ventromedial hypothalamus—turned out to be an assembly of roughly 5,000 neurons, all marbled together, some of them seemingly connected to copulating and others to fighting.

“There’s no such thing as a generic neuron,” says Anderson, who estimates that there may be up to 10,000 distinct classes of neurons in the brain. Even tiny regions of the brain contain a mixture, he says, and these neurons “often influence behavior in different, opposing directions.” In the case of the hypothalamus, some of the neurons seemed to become active during aggressive behavior, some of them during mating behavior, and a small subset—about 20 percent—during both fighting and mating.

That was a provocative discovery, but it was also a relic of old-style neuroscience. Being active was not the same as causing the behavior; it was just a correlation. How did the scientists know for sure what was triggering the behavior? Could they provoke a mouse to pick a fight simply by tickling a few cells in the hypothalamus?

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