Thanks for the Memories

English

fMRI

 
 
How easy is it to falsify memories? New research at the Weizmann Institute shows that a bit of social pressure may be all that is needed. The study, which appeared recently in Science, reveals a unique pattern of brain activity when false memories are formed – one that hints at a surprising connection between our social selves and memory.

The experiment, conducted by Prof. Yadin Dudai and research student Micah Edelson of the Institute’s Neurobiology Department, together with Prof. Raymond Dolan and Dr. Tali Sharot of University College London, took place in four stages. In the first, volunteers watched a documentary film in small groups. Three days later, they returned to the lab individually to take a memory test, answering questions about the film. They were also asked how confident they were about their answers.

They were later invited back to the lab to retake the test while being scanned in a functional magnetic resonance imager (fMRI) that revealed their brain activity. This time, the subjects were also given a “lifeline”: the supposed answers of the others in their film-viewing group (along with social-media-style photos). Planted among these were false answers to questions the volunteers had previously answered correctly and confidently. After seeing these “planted” responses, the participants conformed to the group, giving incorrect answers nearly 70% of the time.  

But were they simply conforming to perceived social demands, or had their memory of the film actually undergone a change? To find out, the researchers invited the subjects back to the lab to take the memory test once again, telling them that the answers they had previously been fed were not those of their fellow film watchers but random computer generations. In some cases the responses reverted back to the original, correct ones; but close to half remained erroneous, implying that the subjects were relying on false memories implanted in the earlier session.

An analysis of the fMRI data showed differences in brain activity between the persistent false memories and the temporary errors of social compliance. The most outstanding feature of the false memories was a strong co-activation and connectivity between two brain areas: the hippocampus and the amygdala. The hippocampus is known to play a role in long-term memory formation, while the amygdala, sometimes known as the emotion center of the brain, plays a role in social interaction. The scientists think that the amygdala may act as a gateway connecting the social and the memory processing parts of the brain; its “stamp” may be needed for some types of memories, to give them approval before they get uploaded to the memory bank. Thus social reinforcement could act on the amygdala, persuading our brains to replace a strong memory with a false one.
 
 

 

Prof. Yadin Dudai’s research is supported by the Norman and Helen Asher Center for Human Brain Imaging, which he heads; the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Institute of Brain Research, which he heads; the Marc Besen and the Pratt Foundation, Australia; Lisa Mierins Smith, Canada; the Abe and Kathryn Selsky Memorial Research Project; and Miel de Botton, UK. Prof. Dudai is the incumbent of the Sara and Michael Sela Professorial Chair of Neurobiology.
 
 
fMRI
Life Sciences
English

Fruit Bats Navigate with Internal Maps

English
GPS technology can make our travels easier and more efficient. But for many animals, the ability to successfully navigate a landscape is not just a matter of convenience – their very survival depends on it. Egyptian fruit bats, for instance, fly dozens of kilometers each night to feed on specific fruit trees, making the return trip the same night. To understand how the bats locate individual trees night after night, scientists attached tiny GPS devices to the bats in the first-ever, comprehensive, GPS-based field study of mammal navigation. The results of this study showed that the bats carry around an internal, cognitive map of their home range, based on such visual landmarks as lights or hills. The study, which appears this week in the Proceedings of the National Academy of Sciences (PNAS) online Early Edition, reveals for the first time how mammals find their way around their natural environment.

Many researchers have investigated the navigational skills of other creatures – birds, fish, insects, lobsters, turtles, etc. – but studies of mammalian navigation have been confined to the lab. Unfortunately, lab studies cannot duplicate the large, complex landscapes an animal must navigate in the natural world. The new GPS-based method gives researchers the best of both worlds. This new approach to studying bat navigation was developed by a neurobiologist – Dr. Nachum Ulanovsky of the Weizmann Institute – and an ecologist – Prof. Ran Nathan of the Hebrew University of Jerusalem, together with his student Asaf Tsoar, in collaboration with Giacomo Dell'Omo of Ornis Italica, Italy, and Alexei Vyssotski of ETH Zurich, Switzerland. In a collaborative effort, they developed the devices – each weighing around 10 grams and containing tiny GPS receivers in addition to memory loggers and batteries. They then used the devices to track the movements of Egyptian fruit bats over several consecutive nights.
An Egyption fruit bat is released with a tiny GPS device on its back
 
At first, the researchers collected data as the bats took flight each night from a cave near the Israeli city of Beit Shemesh. These bats flew in a straight line at speeds of 40 km an hour and more – up to 60 kmh – at elevations of hundreds of meters, to trees that were about 12 to 25 km from their cave. They went to the same trees, night after night, even bypassing apparently identical trees that were nearer to home. The data showed that bats’ navigational abilities rival those of homing pigeons.

The fact that the bats bypassed similar fruit trees to get to their favorite feeding site ruled out smell as their main navigational aid, while an analysis of the data suggested that the bats were not simply “beaconing” on any visual or other individual cue. To investigate further, the scientists took some of the bats to a new area 44 kilometers south of their normal range. Some bats were released at dusk; others were fed in the new area and released just before dawn. Those released first had no trouble navigating to their favorite fruit trees, returning straight back to their caves afterward, while those who were fed first simply made a beeline back to the cave once they were released. Based on a spatial model analysis, as well as discussions with pilots, it appeared that the bats might have been able to see familiar visual landmarks – hills or the lights of human settlements – from this release site.

To prevent them from using visual landmarks as guides, the researchers removed the bats even further south, to a natural depression that limited their field of vision: the Large Crater, located some 84 km south of their cave. Here, some of the bats were released from a hilltop at the edge of the crater and others were let go at the crater’s bottom. Despite the distance, those flying from the hilltop oriented themselves right away and flew back to the cave. The bats inside the crater, however, appeared disoriented, wandering for quite a while before finding their way out of the crater and back to the cave. This confirmed the idea that bats use visual information from a “bird’s eye view” to construct a cognitive map of a wide area. Navigational cues include these distant landmarks, and the scientists believe that the bats most likely compute their location by employing a form of triangulation based on the different azimuths to known distant landmarks.

Because most of the bats released in the crater, when they finally left, exited to the north (the direction of home), Nathan, Ulanovsky and Tsoar believe that the bats may have an additional, back-up navigational mechanism to help when landmarks are unreliable. This mechanism might involve sensing the magnetic fields or directional odors carried on the sea breeze from the Mediterranean.
 
Although lab experiments based on distances of a meter or two had hinted at the existence of an internal map for navigation, this study is the first to show that such mammals as fruit bats use these maps to find their way around areas 100 km in size.
 
 

 
Dr. Nachum Ulanovsky’s research is supported by the Nella and Leon Benoziyo Center for Neurological Diseases; the Clore Center for Biological Physics; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Irving B. Harris Foundation; and the estate of Fannie Sherr.
An Egyption fruit bat is released with a tiny GPS device on its back
Life Sciences
English

Complex Grammar

English
10-08-2011
Two-, three- and four-way retinal neuron interactions on viewing a natural scene
 

Dr. Elad Schneidman of the Weizmann Institute’s Neurobiology Department likens studying how neurons in the brain communicate to learning a new language just by listening to a native speaker. At first the task seems insurmountable, but little by little we begin to pick up on basic words and phrases that repeat themselves. By the time we understand a thousand or so words, we also have a primitive grasp of the grammar and can incorporate new words as we learn them.


Much of our knowledge about the brain has come from studying the “letters” or even “words” of single neuron activity, usually by  measuring the electrical spikes of single neurons or neuron pairs in experiments. This is a bit like trying to understand an entire lecture from hearing a handful of random words. The really interesting “conversation,” says Schneidman, arises between larger groups of neurons. To get at the underlying rules governing neural communication and collective behavior, he looks at activity patterns in networks of around one hundred neurons and tries to understand their interactions.

Few studies deal with the detailed nature of such large groups of neurons. Aside from the experimental challenge, the difficulty is that even 100 neurons present a huge abundance of possible activity patterns – on the order of 1030 . Extracting meaningful information from such a network would seem to be an impractical proposition, at best.

Schneidman and his research student Elad Ganmor, together with Dr. Ronen Segev of Ben-Gurion University of the Negev, approached the problem by combining experimentation and mathematical modeling. The experiments involved fully functional pieces of salamander retina. In each two-millimeter square of tissue, around 100 nerve cells could be reliably recorded. The researchers showed these retina patches film clips of natural scenes and watched as the neurons fired off messages in short spikes of electricity. “These retinal neuron spikes,” says Schneidman, “are the output of the ‘computation’ that the retina performs on the visual input, which would then be sent to the brain. The retina is thus an extension of the brain, and its cellular communication is the same as that of brain cells. We can see unique activity patterns emerge from the ‘chatter’ as the network is exposed to the different scenes. Interestingly, the patterns we see in the retina networks have a specific ‘grammar’ that appears to hold only for natural scenes; not for white noise movies or other unnatural images shown to them.”
 
Dr. Elad Schneidman. Basic communication
 
To reveal some of the ground rules for neuron activity, the scientists used a mathematical model similar to one commonly used in physics, where it was developed to study the behavior of large numbers of magnets in magnetic fields. An equivalent model is also used in statistics and in machine learning. In all these domains, complex behavior arises from pair-wise interactions between elements – attraction and repulsion in magnets, on and off states in binary variables, firing and silence in neurons. When the scientists first applied the model to small networks, it fit perfectly. Even for large networks, the experimental data seemed to fit fairly well, except for a few points that fell off the scale. Upon closer inspection, however, they realized that the data points that didn’t conform to the model belonged to the most frequently occurring activity patterns, and these reflected more complex grammar. In particular, they reflected dependencies between cells that could not be explained by pair relations alone. As a result, their model was good at predicting the rare “phrases” but less accurate when it came to the common ones. But just as we must learn to say: “I am hungry,” before we progress to ordering a full meal with wine, side dishes and dessert in a restaurant, Schneidman and his team realized that they couldn’t ignore the everyday expressions used in brain communication if they wanted to get a feel for its language. Their challenge was to find a way to deal with the common patterns and the rare ones at the same time.

Surprisingly, making a small change in the mathematical formula led to a very simple and accurate way to infer the grammar of this complex system. The original physics equation encodes the interactions between magnets with the numbers 1 and -1. Instead of representing a silent neuron with a -1 – as though it were a negative magnetic pole – they used a 0. While this may seem to be a mere “accounting” issue, it has a profound effect on the formula’s terms in one special case: that in which the elements in the network are only rarely active. This is exactly the situation in the brain: Most neurons are silent most of the time. Suddenly the common phrases could be interpreted, revealing fundamental interactions between neurons. Differences among the various phrases also enabled the researchers to infer different rules from each of the common patterns.

In fact, from an incredibly complex network of possible interactions, the researchers obtained a picture of basic neural communication that is decidedly sparse, yet extremely accurate. “We could assemble a basic grammar of millions of activity patterns from about 500 common phrases that rely on two-, three- and four-way connections – provided we knew which examples to choose,” says Schneidman. “The grammar of neuron networks is eminently learnable.” He thinks it may be learnable precisely because it seems to work like language. The common, constantly repeated phrases may be the way that neurons gain their communications skills and continue to understand one another.

With this new insight into the nature of neural communication, the researchers were able to decode the visual information carried by large groups of retinal cells. Schneidman believes that this new approach could enable us to obtain a detailed picture of the workings of large groups of neurons in different parts of the brain. This might, eventually, lead the way to reading the information encoded in such networks and point to new approaches to treating neurological disorders.
 
Dr. Elad Schneidman's research is supported by the Jeanne and Joseph Nissim Foundation for Life Sciences Research; the Peter and Patricia Gruber Award; and the J&R Foundation.
 
 

 
 
Two-, three- and four-way retinal neuron interactions on viewing a natural scene
Life Sciences
English

Weak Synchronization in Toddler Brains May Be a Biological Marker for Autism

English
 
The biological causes of autism are still not understood. A diagnosis of autism is only possible after ages three or four; and the tests are subjective, based on behavioral symptoms. Now, in research that appeared in Neuron, scientists at the Weizmann Institute of Science, Carnegie Mellon University and the University of California, San Diego have found, for the first time, a method that can accurately identify a biological sign of autism in very young toddlers. By scanning the brain activity of sleeping children, the scientists discovered that the autistic brains exhibited significantly weaker synchronization between brain areas tied to language and communication, compared to that of non-autistic children.

“Identifying biological signs of autism has been a major goal for many scientists around the world, both because they may allow early diagnosis, and because they can provide researchers with important clues about the causes and development of the disorder,” says postdoctoral fellow Dr. Ilan Dinstein, a member of the group of Prof. Rafael Malach, who headed this study in the Weizmann Institute’s Neurobiology Department. While many scientists believe that faulty lines of communication between different parts of the brain are involved in the spectrum of autism disorders, there was no way to observe this in very young children, who are unable to lie still inside an fMRI scanner while they are awake.

But work by Malach’s group and other research groups pointed to a solution. Their studies had shown that even during sleep, the brain does not actually switch off. Rather, the electrical activity of the brain cells switches over to spontaneous fluctuation. These fluctuations are coordinated across the two hemispheres of the brain such that each point on the left is synchronized with its corresponding point in the right hemisphere.

In sleeping autistic toddlers, the fMRI scans showed lowered levels of synchronization between the left and right brain areas known to be involved in language and communication. This pattern was not seen either in children with normal development or in those with delayed language development who were not autistic. In fact, the researchers found that this synchronization was strongly tied to the autistic child’s ability to communicate: The weaker the synchronization, the more severe were the symptoms of autism. On the basis of the scans, the scientists were able to identify 70% of the autistic children between the ages of one and three.

Dinstein: “This biological measurement could help diagnose autism at a very early stage. The goal for the near future is to find additional markers that can improve the accuracy and the reliability of the diagnosis.”   
 
As compared to the control brain (top), the autistic brain (bottom) shows weaker inter-hemispheric synchronization in several areas, particularly the superior temporal gyrus (light blue) and the inferior frontal gyrus (red)
 
 
Prof. Rafael Malach’s research is supported by the Nella and Leon Benoziyo Center for Neurosciences, which he heads; the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Friends of Dr. Lou Siminovitch; and the S. and J. Lurje Memorial Foundation. Prof. Malach is the recipient of the Helen and Martin Kimmel Award for Innovative Investigation. Prof. Malach is the incumbent of the Barbara and Morris L. Levinson Professorial Chair in Brain Research.


 
As compared to the control brain (top), the autistic brain (bottom) shows weaker inter-hemispheric synchronization in several areas, particularly the superior temporal gyrus (light blue) and the inferior frontal gyrus (red)
Life Sciences
English

Senses under Stress: Adversity Blurs Perception

English

 

Jennifer Resnik and Dr. Rony Paz. Differences in perception
 

 

 

 

 

 

 

 

 

 

 

Adversity, we are told, heightens our senses, imprinting sights and sounds precisely in our memories. But recent Weizmann Institute research, which appeared in Nature Neuroscience, suggests the exact opposite may be the case: Perceptions learned in an aversive context are not as sharp as those learned in other circumstances. The findings, which hint that this tendency is rooted in our species’ evolution, may help to explain how post-traumatic stress syndrome and other anxiety disorders develop in some people.


To investigate learning in unfavorable situations, Dr. Rony Paz of the Institute’s Neurobiology Department, together with his student Jennifer Resnik, had volunteers learn that some tones led to an offensive outcome (e.g., a very bad odor), whereas other tones were followed by pleasant a outcome or by nothing at all. The volunteers were later tested for their perceptual thresholds – that is, how well they were able to distinguish either the “bad” or “good” tones from other, similar tones.

As expected from previous studies, in the neutral or positive conditions, the volunteers became better with practice at discriminating between tones. But, surprisingly, when they found themselves exposed to a negative, possibly disturbing stimulus, their performance worsened.

The differences in learning were in fact very basic differences in perception. After learning that a stimulus is associated with a highly unpleasant experience, the subjects could not distinguish it from other, similar stimuli, even though they could do so beforehand or in normal conditions. In other words, no matter how well they usually learned new things, the subjects receiving the “aversive reinforcement” experienced the two tones as the same.
 
 

Evolution and post-traumatic stress syndrome

Paz: “A reduced ability to distinguish between stimuli likely made sense in our evolutionary past: If you’ve previously heard the sound of a lion attacking, your survival might depend on a similar noise sounding the same to you – and pushing the same emotional buttons. Your instincts, then, will tell you to run rather than to consider whether that sound was indeed identical to the growl of the lion the other day.”

Paz believes that this tendency might be stronger in people suffering from post-traumatic stress syndrome. As an example, he points to the 9/11 terror attacks in New York. Many of those who witnessed the strikes on the towers developed post-traumatic stress syndrome, which, in many cases, could be triggered by the sight of tall buildings. Intellectually, they might know that the building before them bore little resemblance to the destroyed towers; but on a more fundamental, instinctive level, they might perceive all tall buildings as being the same and thus associate them with terrifying destruction.

The scientific team is now investigating this idea in continuing research, in which they hope, among other things, to identify the areas in the brain involved in setting the different levels of perception. Paz: “We think this is a trick of the brain that evolved to help us cope with threats but is now dysfunctional in many cases. Besides revealing this very basic aspect of human perception, we hope to shed light on the development of such anxiety disorders as post-traumatic stress syndrome.”
 
Dr. Rony Paz's research is supported by the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Kahn Family Research Center for Systems Biology of the Human Cell; the Ruth and Herman Albert Scholars Program for New Scientists; Pascal and Ilana Mantoux, Israel; Katy and Gary Leff, Calabasas, CA; the Candice Appleton Family Trust; Sam Revusky, Canada; and Dr. and Mrs. Alan Leshner, Potomac, MD. Dr. Paz is the incumbent of the Beracha Foundation Career Development Chair. 

 
 
Jennifer Resnik and Dr. Rony Paz. Differences in perception
Life Sciences
English

Thanks for the Memories

English
 
How easy is it to falsify memory? New research at the Weizmann Institute shows that a bit of social pressure may be all that is needed. The study, which appears Friday in Science, reveals a unique pattern of brain activity when false memories are formed – one that hints at a surprising connection between our social selves and memory.
 
The experiment, conducted by Prof. Yadin Dudai and research student Micah Edelson of the Institute’s Neurobiology Department with Prof. Raymond Dolan and Dr. Tali Sharot of University College London, took place in four stages. In the first, volunteers watched a documentary film in small groups. Three days later, they returned to the lab individually to take a memory test, answering questions about the film. They were also asked how confident they were in their answers.
 
 
 
 
They were later invited back to the lab to retake the test while being scanned in a functional MRI (fMRI) that revealed their brain activity. This time, the subjects were also given a “lifeline”: the supposed answers of the others in their film viewing group (along with social-media-style photos). Planted among these were false answers to questions the volunteers had previously answered correctly and confidently. The participants conformed to the group on these “planted” responses, giving incorrect answers nearly 70% of the time.

But were they simply conforming to perceived social demands, or had their memory of the film actually undergone a change? To find out, the researchers invited the subjects back to the lab to take the memory test once again, telling them that the answers they had previously been fed were not those of their fellow film watchers, but random computer generations. Some of the responses reverted back to the original, correct ones, but close to half remained erroneous, implying that the subjects were relying on false memories implanted in the earlier session.

An analysis of the fMRI data showed differences in brain activity between the persistent false memories and the temporary errors of social compliance. The most outstanding feature of the false memories was a strong co-activation and connectivity between two brain areas: the hippocampus and the amygdala. The hippocampus is known to play a role in long-term memory formation, while the amygdala, sometimes known as the emotion center of the brain, plays a role in social interaction. The scientists think that the amygdala may act as a gateway connecting the social and memory processing parts of our brain; its “stamp” may be needed for some types of memories, giving them approval to be uploaded to the memory banks. Thus social reinforcement could act on the amygdala to persuade our brains to replace a strong memory with a false one.
 
 
Prof. Yadin Dudai’s research is supported by the Norman and Helen Asher Center for Human Brain Imaging, which he heads; the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Institute of Brain Research, which he heads; the Marc Besen and the Pratt Foundation, Australia; Lisa Mierins Smith, Canada; Abe and Kathryn Selsky Memorial Research Project; and Miel de Botton, UK. Prof. Dudai is the incumbent of the Sara and Michael Sela Professorial Chair of Neurobiology.
 

 
Life Sciences
English

Getting a Grasp on Memory

English

 

 
Prof. Yadin Dudai, Shiri Ron, Shoshi Hazvi, Reut Shema, Dr. Alon Chen and Sharon Haramati. Improved memory
 

 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Long-term memory is a slippery thing. Just how slippery was demonstrated a few years ago by Weizmann Institute scientists, who erased entire memories in rats just by blocking a certain protein in the brain. In other words, memory – even the part we imagine to contain neatly packed files – is in reality a dynamic piece of equipment that must be actively maintained to work. Now these scientists have shown, in research that appeared in Science, that manipulating that same protein can enhance memory.

The protein – PKMzeta – is produced in the brain in response to learning, and it acts on the synapses – the active contact points between neurons. It continues to operate there long after the memory has been formed, suggesting that its function is tied not to learning (that is, absorbing information) but to keeping what is learned available in the long-term memory. In 2007, Prof. Yadin Dudai and research student Reut Shema of the Neurobiology Department, together with Prof. Todd Sacktor of SUNY Downstate Medical Center, New York, trained rats to avoid a specific taste and then blocked the activity of PKMzeta in their brains. While the control rats still had a strong aversion to the taste even months after the training, those in which the activity of the protein was briefly blocked had no such qualms, appearing to have forgotten what they had learned.
 
 
Overexpression of PKMzeta in the insular cortex. A merged picture of a neuron stained with GFP (green), PKMzeta (blue), and NeuN (red)
 
 
 
But could extra doses of PKMzeta actually improve memory? Investigating this claim turned out to be a more difficult prospect than blocking protein activity. Simply injecting the protein into the rats’ grey matter was not an option, as the brain is built to keep such extraneous material from reaching the neurons. So Dudai, Shema and Sacktor teamed up with Dr. Alon Chen and Sharon Haramati, also of the Neurobiology Department, to create harmless viruses that carry extra copies of the PKMzeta gene into the brain cells’ nucleus, tricking the neurons themselves into producing greater quantities of the protein.

Once again, they trained the rats to avoid the taste. Weeks after the training, the rats whose brains were churning out more of the protein were much more likely to avoid the taste. In other words, an excess of PKMzeta effectively enhanced their memories. This is the very first demonstration that memories formed long ago can be augmented by manipulating a component of the memory machinery in the brain.

While the technique they developed is suitable only for the lab, the researchers hope that by shedding light on the function of this key component of the memory machinery their findings might eventually point to ways of preventing or treating memory loss. Shema: “Our research is evidence that the brain is very plastic – even long-term memories can be augmented.”
 
Prof. Yadin Dudai's research is supported by the Nella and Leon Benoziyo Center for Neurological Diseases; the Abe and Kathryn Selsky Memorial Research Project; Miel de Botton Aynsley, UK; Dr. Henry Kaminer, New York, NY; Marla L. Schaefer, New York, NY; and Lisa Mierins Smith, Canada. Prof. Dudai is the incumbent of the Sara and Michael Sela Professorial Chair of Neurobiology. 
 

Dr. Alon Chen's research is supported by the Nella and Leon Benoziyo Center for Neurosciences; the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Irwin Green Alzheimer's Research Fund; the Mark Besen and the Pratt Foundation, Australia; Roberto and Renata Ruhman, Brazil; and Martine Turcotte, Canada. Dr. Chen is the incumbent of the Philip Harris and Gerald Ronson Career Development Chair.
 
 
 
Prof. Yadin Dudai, Shiri Ron, Shoshi Hazvi, Reut Shema, Dr. Alon Chen and Sharon Haramati. Improved memory
Life Sciences
English

New Insight into “Aha” Memories

English

When we suddenly get the answer to a riddle or understand the solution to a problem, we can practically feel the light bulb click on in our head. But what happens after the “Aha!” moment? Why do the things we learn through sudden insight tend to stick in our memory?


“Much of memory research involves repetitive, rote learning,” says Kelly Ludmer, a research student in the group of Prof. Yadin Dudai of the Institute’s Neurobiology Department, “but in fact, we regularly absorb large blocks of information in the blink of an eye and remember things quite well from single events. Insight is an example of a one-time event that is often well-preserved in memory.”

To investigate how lessons we gain from insight get embedded in our long-term memory, Ludmer, Dudai and Prof. Nava Rubin of New York University designed a test with “camouflage images” – photographs that had been systematically degraded until they resembled inkblots. When volunteers first viewed the images, they were hard-pressed to identify them. But after the camouflage switched with the original, undoctored picture for a second, the subjects experienced an “Aha!” moment – the image now popped out clearly even in the degraded photograph. Their perceptions, says Ludmer, underwent a sudden change – just as a flash of insight instantly shifts our world view. To tax their memory of the insightful moment, participants were asked to repeat the exercise with dozens of different images and, in a later, repeat session, they were given only the camouflaged images (together with some they hadn’t seen before) to identify.
 
 

Mouse over "camouflage" image for undoctored picture
 


The team found that some of the memories disappeared over time, but the ones that made it past a week were likely to remain. All in all, about half of all the learned “insights” seemed to be consolidated in the subjects’ memories.


To reveal what occurs in the brain at the moment of insight, the initial viewing session was conducted in a functional MRI (fMRI) scanner. When the scientists looked at the fMRI results, they were surprised to find that among the areas that lit up in the scans – those known to be involved in object recognition, for instance – was the amygdala. The amygdala is more famously known as the seat of emotion in the brain. Though it has recently been found to play a role in the consolidation of certain memories, studies have implied that it does so by attaching special weight to emotion-laden events. But the images used in the experiment – hot-air balloons, dogs, people looking through binoculars, etc. – were hardly the sort to elicit an emotional response. Yet not only was the amygdala lighting up in the fMRI, the team found that its activity was actually predictive of the subject’s ability to identify the degraded image long after that moment of induced insight in which it was first recognized.

“Our results demonstrate, for the first time, that the amygdala is important for creating long-term memories – not only when the information learned is explicitly emotional, but also when there is a sudden reorganization of information in our brain, for example, involving a sudden shift in perception,” says Ludmer. “It might somehow evaluate the event, ‘deciding’ whether it is significant and therefore worthy of preservation.”
 
Prof. Yadin Dudai's research is supported by the Nella and Leon Benoziyo Center for Neurological Diseases; the Abe and Kathryn Selsky Memorial Research Project; Miel de Botton Aynsley, UK; Dr. Henry Kaminer, New York, NY; Marla L. Schaefer, New York, NY; and Lisa Mierins Smith, Canada. Prof. Dudai is the incumbent of the Sara and Michael Sela Professorial Chair of Neurobiology. 
 
Mouse over "camouflage" image for undoctored picture
Life Sciences
English

Weizmann Institute scientists show: How Adversity Dulls Our Perceptions

English
 
Adversity, we are told, heightens our senses, imprinting sights and sounds precisely in our memories. But new Weizmann Institute research, which appeared in Nature Neuroscience this week, suggests the exact opposite may be the case: Perceptions learned in an aversive context are not as sharp as those learned in other circumstances. The findings, which hint that this tendency is rooted in our species’ evolution, may help to explain how post-traumatic stress syndrome and other anxiety disorders develop in some people.

To investigate learning in unfavorable situations, Dr. Rony Paz of the Institute’s Neurobiology Department, together with his student Jennifer Resnik, had volunteers learn that some tones lead to an offensive outcome (e.g. a very bad odor), whereas other tones are followed by pleasant a outcome, or else by nothing. The volunteers were later tested for their perceptual thresholds – that is, how well they were able to distinguish either the “bad” or “good” tones from other similar tones.
 
As expected from previous studies, in the neutral or positive conditions, the volunteers became better with practice at discriminating between tones. But surprisingly, when they found themselves exposed to a negative, possibly disturbing stimulus, their performance worsened.
 
The differences in learning were really very basic differences in perception. After learning that a stimulus is associated with highly unpleasant experience, the subjects could not distinguish it from other similar stimuli, even though they could do so beforehand, or in normal conditions. In other words, no matter how well they normally learned new things, the subjects receiving the “aversive reinforcement” experienced the two tones as the same.
 
Paz: “This likely made sense in our evolutionary past: If you’ve previously heard the sound of a lion attacking, your survival might depend on a similar noise sounding the same to you – and pushing the same emotional buttons. Your instincts, then, will tell you to run, rather than to consider whether that sound was indeed identical to the growl of the lion from the other day.”
 
Paz believes that this tendency might be stronger in people suffering from post-traumatic stress syndrome. As an example, he points to the 9-11 terror attacks in New York. Many of those who witnessed the strikes on the towers developed post-traumatic stress syndrome, which, for many of them, can be triggered by tall buildings. Intellectually, they may know the building before them bears little similarity to the destroyed towers, but on a more fundamental, instinctive level, they might perceive all tall buildings to be the same and thus associate them with terrifying destruction.
 
The scientific team is now investigating this idea in continuing research, in which they hope, among other things, to identify the areas in the brain that are involved in setting the different levels of perception. Paz: “We think this is a trick of the brain that evolved to help us cope with threats, but is now dysfunctional in many cases. Besides revealing this very basic aspect of our perception, we hope to shed light on the development of such anxiety disorders as post-traumatic stress syndrome.”
 
Survival in the face of adversity
 
 

Dr. Rony Paz’s research is supported by the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Kahn Family Research Center for Systems Biology of the Human Cell; the Ruth and Herman Albert Scholars Program for New Scientists; the Candice Appleton Family Trust; the Abraham and Sonia Rochlin Foundation; Katy and Gary Leff, Calabasas, CA; Pascal and Ilana Mantoux, Israel; and Sam Revusky, Canada. Dr. Paz is the incumbent of the Beracha Foundation Career Development Chair.

 a lion. Survival in the face of adversity
Life Sciences
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Anti-Stress Proteins

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(l-r) Dr. Alon Chen, Gili Ezra-Nevo, Dr. Evan Elliott, Adi Neufeld Cohen and Dr. Michael Tsoory. Relieving stress
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stress and anxiety are normal: They evolved to help us deal with daily threats to our existence. But the stress response – pounding heart, tensed muscles, sweating palms – is meant to shut down after the threat has passed. People who have a hard time “turning off” their stress response, often as a result of psychological trauma, can develop post-traumatic stress syndrome, as well as anorexia, anxiety disorders or depression.

How does the body recover from its response to shock or acute stress? This question is at the heart of research conducted by Dr. Alon Chen of the Institute’s Neurobiology Department. The response begins in the brain, and Chen concentrates on a family of proteins that play a prominent role in regulating this mechanism. One protein in the family – CRF – is known to initiate a chain of events that occurs when we cope with pressure, and scientists have hypothesized that other members of the family are involved in shutting down that chain. In research that appeared in the Proceedings of the National Academy of Sciences (PNAS), Chen and his team have now, for the first time, provided sound evidence that three family members known as urocortin 1, 2 and 3 – are responsible for turning off the stress response.

The research group, including Adi Neufeld Cohen, Dr. Michael Tsoory, Dmitriy Getselter and Shosh Gil, created genetically engineered mice that don’t produce the three urocortin proteins. Before they were exposed to stress, these mice acted just like the control mice, showing no unusual anxiety. When the scientists stressed the mice, both groups reacted in the same way, showing clear signs of distress. Differences between the groups appeared only when they were checked 24 hours after the stressful episode: While the control mice had returned to their normal behavior, appearing to have recovered completely from the shock, the engineered mice were still showing the same levels of anxiety the scientists had observed immediately following their exposure to the stress.
 
cultured Cultured nerve cells that have been inoculated with RNA-bearing viruses. This RNA targets the CRF stress response, reducing gene expression
 
Clearly, the urocortin proteins are crucial for returning the body to normal, but how, exactly, do they do this? To identify the mechanism for the proteins’ activity, Chen and his team tested both groups of mice for expression levels of a number of genes known to be involved in the stress response. They found that gene expression levels remained constant both during and after stress in the engineered mice. In contrast, patterns of gene expression in the control mice showed quite a bit of change 24 hours after the event. In other words, without the urocortin system, the “return to normal” program couldn’t be activated, and the stress genes continued to function.
 
Chen: “Our findings imply that the urocortin system plays a central role in regulating stress responses, and this may have implications for anxiety disorders, depression, anorexia and other conditions. The genetically engineered mice we created could be effective research models for these diseases.”
 
Dr. Alon Chen's research is supported by the Nella and Leon Benoziyo Center for Neurosciences; the Nella and Leon Benoziyo Center for Neurological Diseases; the Carl and Micaela Einhorn-Dominic Brain Research Institute; the Irwin Green Alzheimer's Research Fund; the Mark Besen and the Pratt Foundation, Australia; Roberto and Renata Ruhman, Brazil; and Martine Turcotte, Canada. Dr. Chen is the incumbent of the Philip Harris and Gerald Ronson Career Development Chair. 
 
cultured Cultured nerve cells that have been inoculated with RNA-bearing viruses. This RNA targets the CRF stress response, reducing gene expression
Life Sciences
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