How to Learn math without fear, Stanford expert says

Stanford Prof. Boaler finds that children who excel in math learn to develop "number sense," which is much different from the memorization that is often stressed in school.
Image Credit: THEPLANETWALL STOCK

Students learn math best when they approach the subject as something they enjoy, according to a Stanford education expert. Speed pressure, timed testing and blind memorization pose high hurdles in the youthful pursuit of math.

"There is a common and damaging misconception in mathematics – the idea that strong math students are fast math students," said Jo Boaler, a Stanford professor of mathematics education and the lead author on a new working paper. Boaler's co-authors are Cathy Williams, cofounder of Stanford'sYouCubed, and Amanda Confer, a Stanford graduate student in education. 

Curriculum timely

Fortunately, said Boaler, the new national curriculum standards known as the Common Core Standards for K-12 schools de-emphasize the rote memorization of math facts. Maths facts are fundamental assumptions about math, such as the times tables (2 x 2 = 4), for example. Still, the expectation of rote memorization continues in classrooms and households across the United States.

While research shows that knowledge of math facts is important, Boaler said the best way for students to know math facts is by using them regularly and developing understanding of numerical relations. Memorization, speed and test pressure can be damaging, she added.

On the other hand, people with "number sense" are those who can use numbers flexibly, she said. For example, when asked to solve the problem of 7 x 8, someone with number sense may have memorized 56, but they would also be able to use a strategy such as working out 10 x 7 and subtracting two 7s (70-14).

"They would not have to rely on a distant memory," Boaler wrote.

In fact, in one research project the investigators found that the high-achieving students actually used number sense, rather than rote memory, and the low-achieving students did not.

The conclusion was that the low achievers are often low achievers not because they know less but because they don't use numbers flexibly.

"They have been set on the wrong path, often from an early age, of trying to memorize methods instead of interacting with numbers flexibly," she wrote. Number sense is the foundation for all higher-level mathematics, she noted. 

Role of the brain

Boaler said that some students will be slower when memorizing, but still possess exceptional mathematics potential.

"Math facts are a very small part of mathematics, but unfortunately students who don't memorize math facts well often come to believe that they can never be successful with math and turn away from the subject," she said.

Prior research found that students who memorized more easily were not higher achieving – in fact, they did not have what the researchers described as more "math ability" or higher IQ scores. Using an MRI scanner, the only brain differences the researchers found were in a brain region called the hippocampus, which is the area in the brain responsible for memorizing facts – the working memory section.

But according to Boaler, when students are stressed – such as when they are solving math questions under time pressure – the working memory becomes blocked and the students cannot as easily recall the math facts they had previously studied. This particularly occurs among higher achieving students and female students, she said.

Some estimates suggest that at least a third of students experience extreme stress or "math anxiety" when they take a timed test, no matter their level of achievement. "When we put students through this anxiety-provoking experience, we lose students from mathematics," she said.

Boaler contrasts the common approach to teaching math with that of teaching English. In English, a student reads and understands novels or poetry, without needing to memorize the meanings of words through testing. They learn words by using them in many different situations – talking, reading and writing.

"No English student would say or think that learning about English is about the fast memorization and fast recall of words," she added.

Strategies, activities 

In her paper, "Fluency without Fear," Boaler provides activities for teachers and parents that help students learn math facts at the same time as developing number sense. These include number talks, addition and multiplication activities, and math cards.

Importantly, she said, these activities include a focus on the visual representation of number facts. When students connect visual and symbolic representations of numbers, they are using different pathways in the brain, which deepens their learning, as shown by recent brain research.

"Math fluency" is often misinterpreted, with an over-emphasis on speed and memorization, she said. "I work with a lot of mathematicians, and one thing I notice about them is that they are not particularly fast with numbers; in fact some of them are rather slow. This is not a bad thing; they are slow because they think deeply and carefully about mathematics."

She refers to the famous French mathematician, Laurent Schwartz, who wrote in his autobiography that he often felt stupid in school, as he was one of the slowest math thinkers in class.
Math anxiety and fear play a big role in students dropping out of mathematics, said Boaler.

"When we emphasize memorization and testing in the name of fluency we are harming children, we are risking the future of our ever-quantitative society and we are threatening the discipline of mathematics. We have the research knowledge we need to change this and to enable all children to be powerful mathematics learners. Now is the time to use it," she said.

Source: Standford Unversity

Why Do We Feel Thirst? An Interview with Yuki Oka

Credit: Lance Hayashida/Caltech Marketing and Communications

To fight dehydration on a hot summer day, you instinctively crave the relief provided by a tall glass of water. But how does your brain sense the need for water, generate the sensation of thirst, and then ultimately turn that signal into a behavioral trigger that leads you to drink water? That's what Yuki Oka, a new assistant professor of biology at Caltech, wants to find out.

Oka's research focuses on the study of how the brain and body work together to maintain a healthy ratio of salt to water as part of a delicate form of biological balance called homeostasis.

Recently, Oka came to Caltech from Columbia University. We spoke with him about his work, his interests outside of the lab, and why he's excited to be joining the faculty at Caltech.

Can you tell us a bit more about your research?

The goal of my research is to understand the mechanisms by which the brain and body cooperate to maintain our internal environment's stability, which is called homeostasis. I'm especially focusing on fluid homeostasis, the fundamental mechanism that regulates the balance of water and salt. When water or salt are depleted in the body, the brain generates a signal that causes either a thirst or a salt craving. And that craving then drives animals to either drink water or eat something salty.

I'd like to know how our brain generates such a specific motivation simply by sensing internal state, and then how that motivation—which is really just neural activity in the brain—goes on to control the behavior.

Why did you choose to study thirst?

After finishing my Ph.D. in Japan, I came to Columbia University where I worked on salt sensing mechanisms in the mammalian taste system. We found that the peripheral taste system has a key function for salt homeostasis in the body by regulating our salt intake behavior. But of course, the peripheral sensor does not work by itself.  It requires a controller, the brain, which uses information from the sensor. So I decided to move on to explore the function of the brain; the real driver of our behaviors.

I was fascinated by thirst because the behavior it generates is very robust and stereotyped across various species. If an animal feels thirst, the behavioral output is simply to drink water. On the other hand, if the brain triggers salt appetite, then the animal specifically looks for salt—nothing else. These direct causal relations make it an ideal system to study the link between the neural circuit and the behavior.

You recently published a paper on this work in the journal Nature. Could you tell us about those findings?

In the paper, we linked specific neural populations in the brain to water drinking behavior. Previous work from other labs suggested that thirst may stem from a part of the brain called the hypothalamus, so we wanted to identify which groups of neurons in the hypothalamus control thirst. Using a technique called optogenetics that can manipulate neural activities with light, we found two distinct populations of neurons that control thirst in two opposite directions. When we activated one of those two populations, it evoked an intense drinking behavior even in fully water-satiated animals. In contrast, activation of a second population drastically suppressed drinking, even in highly water-deprived thirsty animals.  In other words, we could artificially create or erase the desire for drinking water.

Our findings suggest that there is an innate brain circuit that can turn an animal's water-drinking behavior on and off, and that this circuit likely functions as a center for thirst control in the mammalian brain. This work was performed with support from Howard Hughes Medical Institute and National Institutes of Health [for Charles S. Zuker at Columbia University, Oka's former advisor].

You use a mouse model to study thirst, but does this work have applications for humans?

There are many fluid homeostasis-associated conditions; one example is dehydration. We cannot specifically say a direct application for humans since our studies are focused on basic research. But if the same mechanisms and circuits exist in mice and humans, our studies will provide important insights into human physiologies and conditions.

Where did you grow up—and what started your initial interest in science?

I grew up in Japan, close to Tokyo, but not really in the center of the city. It was a nice combination between the big city and nature. There was a big park close to my house and when I was a child, I went there every day and observed plants and animals. That's pretty much how I spent my childhood. My parents are not scientists—neither of them, actually. It was just my innate interest in nature that made me want to be a scientist.

What drew you to Caltech?

I'm really excited about the environment here and the great climate. That's actually not trivial; I think the climate really does affect the people. For example, if you compare Southern California to New York, it's just a totally different character. I came here for a visit last January, and although it was my first time at Caltech I kind of felt a bond. I hadn't even received an offer yet, but I just intuitively thought, "This is probably the place for me."

I'm also looking forward to talking to my colleagues here who use fMRI for human behavioral research. One great advantage about using human subjects in behavioral studies is that they can report back to you about how they feel. There are certainly advantages of using an animal model, like mice. But they cannot report back. We just observe their behavior and say, "They are drinking water, so they must be thirsty." But that is totally different than someone telling you, "I feel thirsty." I believe that combining advantages of animal and human studies should allow us to address important questions about brain functions.

Do you have any hobbies?

I play basketball in my spare time, but my major hobby is collecting fossils. I have some trilobites and, actually, I have a complete set of bones from a type of herbivorous dinosaur. It is being shipped from New York right now and I may put it in my new office.

Written by Jessica Stoller-Conrad


Source: California Institute of Technology

Existing drug, riluzole, may prevent foggy 'old age' brain, research shows

Better memory makers: When researchers looked at certain neurons (similar to the one shown on top) in rats treated with riluzole, they found an important change in one brain region, the hippocampus: more clusters of so-called spines, receiving connections that extend from the branches of a neuron (bottom). Credit: Image courtesy of Rockefeller University

Forgetfulness, it turns out, is all in the head. Scientists have shown that fading memory and clouding judgment, the type that comes with advancing age, show up as lost and altered connections between neurons in the brain. But new experiments suggest an existing drug, known as riluzole and already on the market as a treatment for ALS, may help prevent these changes.

Researchers at The Rockefeller University and The Icahn School of Medicine at Mount Sinai found they could stop normal, age-related memory loss in rats by treating them with riluzole. This treatment, they found, prompted changes known to improve connections, and as a result, communication, between certain neurons within the brain's hippocampus.

"By examining the neurological changes that occurred after riluzole treatment, we discovered one way in which the brain's ability to reorganize itself -- its neuroplasticity -- can be marshaled to protect it against some of the deterioration that can accompany old age, at least in rodents," says co-senior study author Alfred E. Mirsky Professor Bruce McEwen, head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. The research is published this week in Proceedings of the National Academy of Sciences.

Neurons connect to one another to form circuits connecting certain parts of the brain, and they communicate using a chemical signal known as glutamate. But too much glutamate can cause damage; excess can spill out and excite connecting neurons in the wrong spot. In the case of age-related cognitive decline, this process damages neurons at the points where they connect -- their synapses. In neurodegenerative disorders, such as Alzheimer's disease, this contributes to the death of neurons.

Used to slow the progress of another neurodegenerative condition, ALS (also known as Lou Gehrig's disease), riluzole was an obvious choice as a potential treatment, because it works by helping to control glutamate release and uptake, preventing harmful spillover. The researchers began giving riluzole to rats once they reached 10 months old, the rat equivalent of middle age, when their cognitive decline typically begins.

After 17 weeks of treatment, the researchers tested the rats' spatial memory -- the type of memory most readily studied in animals -- and found they performed better than their untreated peers, and almost as well as young rats. For instance, when placed in a maze they had already explored, the treated rats recognized an unfamiliar arm as such and spent more time investigating it.

When the researchers looked inside the brains of riluzole-treated rats, they found telling changes to the vulnerable glutamate sensing circuitry within the hippocampus, a brain region implicated in memory and emotion.

"We have found that in many cases, aging involves synaptic changes that decrease synaptic strength, the plasticity of synapses, or both," said John Morrison, professor of neuroscience and the Friedman Brain Institute and dean of basic sciences and the Graduate School of Biomedical Sciences at Mount Sinai. "The fact that riluzole increased the clustering of only the thin, most plastic spines, suggests that its enhancement of memory results from both an increase in synaptic strength and synaptic plasticity, which might explain its therapeutic effectiveness."

In this case, the clusters involved thin spines, a rapidly adaptable type of spine. The riluzole-treated animals had more clustering than the young animals and their untreated peers, who had the least. This discovery led the researchers to speculate that, in general, the aged brain may compensate by increasing clustering. Riluzole appears to enhance this mechanism.

"In our study, this phenomenon of clustering proved to be the core underlying mechanism that prevented age-related cognitive decline. By compensating the deleterious changes in glutamate levels with aging and Alzheimer's disease and promoting important neuroplastic changes in the brain, such as clustering of spines, riluzole may prevent cognitive decline," says first author Ana Pereira, an instructor in clinical investigation in McEwen's laboratory.

Taking advantage of the overlap of neural circuits vulnerable to age-related cognitive decline and Alzheimer's disease, Pereira is currently conducting a clinical trial to test the effectiveness of riluzole for patients with mild Alzheimer's.

Source: Rockefeller University

‘Smart’ drugs won’t make smart people smarter, research concludes

Dr. Ahmed Dahir Mohamed is in the School of Psychology at The University of Nottingham Malaysia Campus. Credit: The University of Nottingham

The study carried out by Dr Ahmed Dahir Mohamed, in the School of Psychology at The University of Nottingham Malaysia Campus, and published in the open access journal PLOS ONE, showed the drug had negative effects in healthy people.

Dr Mohamed said: "We looked at how the drug acted when you are required to respond accurately and in a timely manner. Our findings were completely opposite to the results we expected."

In a randomised double blind study, 'Modafinil increases the latency of response in the Hayling Sentence Completion Test in Healthy Volunteers: A Randomised Controlled Trial', they administered 32 participants with the drug and 32 with a placebo. All the participants were given a famous neuropsychological task known as the Hayling Sentence Completion Test in which they were asked to respond both quickly and accurately. Dr Mohamed found the drug slowed down reaction times, impaired their ability to respond in a timely manner and failed to improve their performance of the task.

Dr Mohamed said: "It has been argued that Modafinil might improve your performance by delaying your ability to respond. It has been suggested this 'delay dependent improvement' might improve cognitive performance by making people less impulsive. We found no evidence to support those claims.

"Our research showed that when a task required instant reactions the drug just increased reaction times with no improvement to cognitive performance."

This backs up the findings of a previous study carried out by Dr Mohamed and published in September 2014 in The Journal of Creative Behaviour. The study: The Effects of Modafinil on Convergent and Divergent Thinking of Creativity: A Randomised Controlled Trial showed that the so called 'smart' drug impaired the participant's ability to respond in a creative way particularly when they were asked to respond laterally -- outside the box.

Does Modafinil benefit anyone?

When Dr Mohamed looked at participant's ability to problem solve in a creative manner he found that those who weren't particularly creative to start with were improved by the drug while those who were creative were impaired by the drug. He said: "Our study backs up previous research that suggests psychostimulants improve people at the lower end of the spectrum in cognition whereas they impair people who are at the optimum level of cognitive function -- healthy people for example. It looks like Modafinil is not helpful for healthy individuals and it might even impair their ability to respond and might stifle their lateral thinking, while people who have some sort of deficiency in creativity are helped by the drug."

What can make us smarter?

Ahmed Mohamed's research was carried out while he was at Cambridge University. He has since moved to The University of Nottingham Malaysia Campus where he will be looking at the effects of non-pharmacological interventions, such as meditation, exercise and diet on the healthy brain. He is also currently using Electroencephalography (EEG) to study how mindfulness can affect the healthy adolescent brain.

Dr Mohamed said: "What I have found in my doctoral studies is that if you are already a healthy person and functioning at an optimum level, it is really difficult to improve your cognition. But the brain of the adolescent is still in development and you might be able to improve cognition at this stage of our development through positive interaction, healthy diet or mindfulness."

Source: University of Nottingham

Credit score can also describe health status

It appears the same behaviors that ruin credit ruin health too. Credit: © Ivelin Radkov / Fotolia

A credit score doesn't just reduce a person's entire financial history down to a single number and somehow predict their credit-worthiness.

It might also be saying something about a person's health status, too, according to a new analysis from a long-term study of the physical and mental health of more than 1,000 New Zealanders who have been monitored continuously from birth to age 38.

The latest paper from the study, appearing this week in the Proceedings of the National Academy of Sciences, has found a strong relationship between low credit scores and poor cardiovascular health.

This doesn't mean that poor financial management hurts your health, post-doctoral researcher Salomon Israel of Duke University is quick to point out. It's that the sort of personal attributes that can lead to a poor credit score can also contribute to poor health.

This and other studies from the Dunedin Multidisciplinary Health and Development Study in New Zealand have found that self-control, planning ahead and perseverance are attributes that predict both better financial status and better health.

"What it comes down to is that people who don't take care of their money don't take care of their health," said study leader Terrie Moffitt, who is the Nannerl O. Keohane university professor of psychology and neuroscience at Duke. She said this study confirms what the insurance and financial industries may already understand.

Backtracking into the data on these study participants, the researchers found that about 20% of the relationship between credit scores and heart health was accounted for by the attitudes, behaviors and competencies displayed by the study members when they were younger than age 10.

"We're showing that these things take root early in life," Israel said.

Harvard economist David Laibson, who was not involved in the research, said the study "fundamentally transforms our understanding of the psychological factors that connect our health and wealth."

Lamar Pierce, an associate professor of organization & strategy at Washington University in St. Louis, agreed. "This study is important because it identifies common cognitive foundations long before financial and physical health problems emerge," said Pierce, who was not involved in this study. "It provides hope that early life intervention can impede the development of life-long patterns of illness and financial struggle."

Using a standard measure called the Framingham cardiovascular risk score, the Duke researchers estimated the "heart age" of their participants, based on blood pressure, cholesterol levels, blood sugar and smoking habits. At age 38, the participants' Framingham "heart ages" ranged from 22 to 85 years. Participants with higher credit scores had younger "heart ages." The components of the Dunedin study's human capital measure -- educational attainment, cognitive ability and self-control -- each predicted higher credit scores and younger heart age.

The idea of checking credit scores against the detailed personal data in the Dunedin study came from a conversation Moffitt had with her seatmate on a plane about a decade ago. When she told her travelling companion from the life insurance industry that she studied self-control and life outcomes, he said, "We do that too, but we use credit scores."

"The thing that's so compelling about credit scores is that they're both predictive and retrospective," said co-author Avshalom Caspi, the Edward M. Arnett professor of psychology and neuroscience, psychiatry & behavioral sciences at Duke. "They offer a window on the future, but also a window on the past."

In recent years, credit scores have been used for pre-employment screening and many other functions beyond their original intent, Israel said. This study seems to bear out their usefulness as a proxy for a person's reliability and steadfastness, and in turn how healthy they may be.

"Our findings suggest that life insurance companies that acquire an applicant's credit score are also indirectly acquiring information about that applicant's educational attainment, intelligence and personality, right back to childhood," the authors wrote.

The link might work the other way as well. In less developed countries where credit scores aren't available, a Harvard team has been experimenting with using a 40-minute personality quiz to assess candidates' credit-worthiness for microloans.

This research was supported by the New Zealand Health Research Council, US National Institute on Aging (AG032282, T32-AG000029), the UK Medical Research Council (MR/K00381X) the Jacobs Foundation and the Yad Hanadiv Rothschild Foundation.

Source: Duke University

Lost memories might be able to be restored, suggests research into marine snail

New UCLA research indicates that lost memories can be restored. The findings offer some hope for patients in the early stages of Alzheimer's disease.

New UCLA research indicates that lost memories can be restored. The findings offer some hope for patients in the early stages of Alzheimer's disease.

For decades, most neuroscientists have believed that memories are stored at the synapses -- the connections between brain cells, or neurons -- which are destroyed by Alzheimer's disease. The new study provides evidence contradicting the idea that long-term memory is stored at synapses.

"Long-term memory is not stored at the synapse," said David Glanzman, a senior author of the study, and a UCLA professor of integrative biology and physiology and of neurobiology. 

"That's a radical idea, but that's where the evidence leads. The nervous system appears to be able to regenerate lost synaptic connections. If you can restore the synaptic connections, the memory will come back. It won't be easy, but I believe it's possible."

The findings were published recently in eLife.

Glanzman's research team studies a type of marine snail called Aplysia to understand the animal's learning and memory. The Aplysia displays a defensive response to protect its gill from potential harm, and the researchers are especially interested in its withdrawal reflex and the sensory and motor neurons that produce it.

They enhanced the snail's withdrawal reflex by giving it several mild electrical shocks on its tail. The enhancement lasts for days after a series of electrical shocks, which indicates the snail's long-term memory. Glanzman explained that the shock causes the hormone serotonin to be released in the snail's central nervous system.

Long-term memory is a function of the growth of new synaptic connections caused by the serotonin, said Glanzman, a member of UCLA's Brain Research Institute. As long-term memories are formed, the brain creates new proteins that are involved in making new synapses. If that process is disrupted -- for example by a concussion or other injury -- the proteins may not be synthesized and long-term memories cannot form. (This is why people cannot remember what happened moments before a concussion.)

"If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn't remember the training," 

Glanzman said. "However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later. In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn't affect long-term memory. That's true in the Aplysia and in human's brains." (This explains why people's older memories typically survive following a concussion.)

Glanzman's team found the same mechanism held true when studying the snail's neurons in a Petri dish. The researchers placed the sensory and motor neurons that mediate the snail's withdrawal reflex in a Petri dish, where the neurons re-formed the synaptic connections that existed when the neurons were inside the snail's body. When serotonin was added to the dish, new synaptic connections formed between the sensory and motor neurons. But if the addition of serotonin was immediately followed by the addition of a substance that inhibits protein synthesis, the new synaptic growth was blocked; long-term memory could not be formed.

The researchers also wanted to understand whether synapses disappeared when memories did. To find out, they counted the number of synapses in the dish and then, 24 hours later, added a protein synthesis inhibitor. One day later, they re-counted the synapses.

What they found was that new synapses had grown and the synaptic connections between the neurons had been strengthened; late treatment with the protein synthesis inhibitor did not disrupt the long-term memory. The phenomenon is extremely similar to what happens in the snail's nervous system during this type of simple learning, Glanzman said.

Next, the scientists added serotonin to a Petri dish containing a sensory neuron and motor neuron, waited 24 hours, and then added another brief pulse of serotonin -- which served to remind the neurons of the original training -- and immediately afterward add the protein synthesis inhibitor. This time, they found that synaptic growth and memory were erased. When they re-counted the synapses, they found that the number had reset to the number before the training, Glanzman said. This suggests that the "reminder" pulse of serotonin triggered a new round of memory consolidation, and that inhibiting protein synthesis during this "reconsolidation" erased the memory in the neurons.

If the prevailing wisdom were true -- that memories are stored in the synapses -- the researchers should have found that the lost synapses were the same ones that had grown in response to the serotonin. But that's not what happened: Instead, they found that some of the new synapses were still present and some were gone, and that some of the original ones were gone, too.

Glanzman said there was no obvious pattern to which synapses stayed and which disappeared, which implied that memory is not stored in synapses.

When the scientists repeated the experiment in the snail, and then gave the animal a modest number of tail shocks -- which do not produce long-term memory in a naive snail -- the memory they thought had been completely erased returned. This implies that synaptic connections that were lost were apparently restored.

"That suggests that the memory is not in the synapses but somewhere else," Glanzman said. 

"We think it's in the nucleus of the neurons. We haven't proved that, though."

Glanzman said the research could have significant implications for people with Alzheimer's disease. Specifically, just because the disease is known to destroy synapses in the brain doesn't mean that memories are destroyed.

"As long as the neurons are still alive, the memory will still be there, which means you may be able to recover some of the lost memories in the early stages of Alzheimer's," he said.

Glanzman added that in the later stages of the disease, neurons die, which likely means that the memories cannot be recovered.

The cellular and molecular processes seem to be very similar between the marine snail and humans, even though the snail has approximately 20,000 neurons and humans have about 1 trillion. Neurons each have several thousand synapses.

Glanzman used to believe that traumatic memories could be erased but he has changed his mind. He now believes that, because memories are stored in the nucleus, it may be much more difficult to modify them. He will continue to study how the marine snail's memories are restored and how synapses re-grow.

Co-authors of the study include Shanping Chen, Diancai Cai and Kaycey Pearce, research associates in Glanzman's laboratory.

The research was funded by the National Institutes of Health's National Institute of Neurological Disorders and Stroke, the National Institute of Mental Health and the National Science Foundation.

Almost all the processes that are involved in memory in the snail also have been shown to be involved in memory in the brains of mammals, Glanzman said.

In a 1997 study published in the journal Science, Glanzman and colleagues identified a cellular mechanism in the Aplysia that plays an important role in learning and memory. A protein called N-methyl D-aspartate, or NMDA, receptor enhances the strength of synaptic connections in the nervous system and plays a vital role in memory and in certain kinds of learning in the mammalian brain as well. Glanzman's demonstration that the NMDA receptor plays a critical role in learning in a simple animal like the marine snail was entirely unexpected at the time.

Source: University of California, Los Angeles

No 'bird brains'? Crows exhibit advanced relational thinking, study suggests

Study finds crows spontaneously solve higher-order relational-matching tasks. Credit: Photo courtesy of Lomonosov Moscow University.

Crows have long been heralded for their high intelligence -- they can remember faces, use tools and communicate in sophisticated ways.

But a newly published study finds crows also have the brain power to solve higher-order, relational-matching tasks, and they can do so spontaneously. That means crows join humans, apes and monkeys in exhibiting advanced relational thinking, according to the research.

Russian researcher Anna Smirnova studies a crow making the correct selection during a relational matching trial.

"What the crows have done is a phenomenal feat," says Ed Wasserman, a psychology professor at the University of Iowa and corresponding author of the study. "That's the marvel of the results. It's been done before with apes and monkeys, but now we're dealing with a bird; but not just any bird, a bird with a brain as special to birds as the brain of an apes is special to mammals."

"Crows Spontaneously Exhibit Analogical Reasoning," which was published December 18 in Current Biology, was written by Wasserman and Anna Smirnova, Zoya Zorina and Tanya Obozova, researchers with the Department of Biology at Lomonosov Moscow State University in Moscow, Russia, where the study was conducted.

Wasserman said the Russian researchers have studied bird species for decades and that a main theme of their work is cognition. He credits his counterparts with a thoughtful and well-planned study.

"This was a very artful experiment," Wasserman says. "I was just bowled over by how innovative it was."

The study involved two hooded crows that were at least 2 years old. First, the birds were trained and tested to identify items by color, shape and number of single samples.

Here is how it worked: the birds were placed into a wire mesh cage into which a plastic tray containing three small cups was occasionally inserted. The sample cup in the middle was covered with a small card on which was pictured a color, shape or number of items. The other two cups were also covered with cards -- one that matched the sample and one that did not. During this initial training period, the cup with the matching card contained two mealworms; the crows were rewarded with these food items when they chose the matching card, but they received no food when they chose the other card.

Once the crows has been trained on identity matching-to-sample, the researchers moved to the second phase of the experiment. This time, the birds were assessed with relational matching pairs of items.

These relational matching trials were arranged in such a way that neither test pairs precisely matched the sample pair, thereby eliminating control by physical identity. For example, the crows might have to choose two same-sized circles rather than two different-sized circles when the sample card displayed two same-sized squares.

What surprised the researchers was not only that the crows could correctly perform the relational matches, but that they did so spontaneously--without explicit training.

"That is the crux of the discovery," Wasserman says. "Honestly, if it was only by brute force that the crows showed this learning, then it would have been an impressive result. But this feat was spontaneous."

Still the researchers acknowledge that the crows' relational matching behavior did not come without some background knowledge.

"Indeed, we believe that their earlier IMTS (identity matching-to-sample) training is likely to have enabled them to grasp a broadly applicable concept of sameness that could apply to novel two-item samples and test stimuli involving only relational sameness," the researchers wrote. "Just how that remarkable transfer is accomplished represents an intriguing matter for future study."

Anthony Wright, neurobiology and anatomy professor at the University of Texas-Houston Medical School, says the discovery ranks on par with demonstrations of tool use by some birds, including crows.

"Analogical reasoning, matching relations to relations, has been considered to be among the more so-called 'higher order' abstract reasoning processes," he says. "For decades such reasoning has been thought to be limited to humans and some great apes. The apparent spontaneity of this finding makes it all the more remarkable."

Joel Fagot, director of research at the University of Aix-Marseille in France, agrees the results shatter the notion that "sophisticated forms of cognition can only be found in our 'smart' human species. Accumulated evidence suggests that animals can do more than expected."

Wasserman concedes there will be skeptics and hopes the experiment will be repeated with more crows as well as other species. He suspects researchers will have more such surprises in store for science.

"We have always sold animals short," he says. "That human arrogance still permeates contemporary cognitive science."

Source: University of Iowa