Testing, not studying, makes for strong long-term memories

Blogging on Peer-Reviewed ResearchIt’s a familiar scene – the wee hours of the morning are ticking away and your head is bent over a stack of notes, desperately trying to cram as much knowledge into your head before the test in the morning.

Exam roomBecause of the way our education system works, this process of hard studying has become almost synonymous with the act of learning, and the inevitable tests and exams that bookend this ordeal merely assess how much information has stuck.

But a new study reveals that the tests themselves do more good for our ability to learn that the many hours before them spent relentlessly poring over notes and textbook. The act of repeatedly retrieving and using learned information drives memories into long-term storage, while repetitive revision produced almost no benefits.

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Time doesn’t actually slow down in a crisis

Blogging on Peer-Reviewed ResearchIn The Matrix, when an agent first shoots at Neo, his perception of time slows down, allowing him to see and avoid oncoming bullets. In the real world, almost all of us have experienced moments of crisis when time seems to slow to a crawl, be it a crashing car, an incoming fist, or a falling valuable.

Time doesn’t actually slow down in a crisisNow, a trio of scientists has shown that this effect is an illusion. When danger looms, we don’t actually experience events in slow motion. Instead, our brains just remember time moving more slowly after the event has passed.

Chess Stetson, Matthew Fiesta and David Eagleman demonstrated the illusion by putting a group of volunteers through 150 terrifying feet of free-fall. They wanted to see if the fearful plummet allowed them to successfully complete a task that was only possible if time actually moved more slowly to their eyes.

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Songbirds need so-called “human language gene” to learn new tunes

Blogging on Peer-Reviewed ResearchThe nasal screech of Chris Tucker sound worlds apart from the song of a nightingale but both human speech and birdsong actually have a lot in common. Both infants and chicks learn their respective tongues by imitating others. They pick up new material most easily during specific periods of time as they grow up, they need practice to improve and they pick up local dialects. And as infants unite words to form sentences, so do songbirds learn to combine separate riffs into a full song. Songbirds need so-called “human language gene” to learn new tunes

Because of these similarities, songbirds make a good model for inquisitive neuroscientists looking to understand the intricacies of human speech. Zebra finches are a particularly enlightening species and they have just shown Sebastian Haesler that the so-called human ‘language gene’ FOXP2 also controls an songbird’s ability to pick up new material.

FOXP2 has a long and sordid history of fascinating science and shoddy science writing. It has been consistently mislabelled as “the language gene” and after the discovery that the human and chimp versions differed by just two small changes, it was also held responsible for the evolution of human language. Even though these claims are far-fetched (for reasons I’ll delve into later), there is no doubt that faults in FOXP2 can spell disaster for a person’s ability to speak.

Mutated versions cause a speech impairment called developmental verbal dyspraxia (DVD), where people are unable to coordinate the positions of their jaws, lips, tongues and faces, even though their minds and relevant muscles are in reasonable working order. They’re like an orchestra that plays a cacophony despite having a decent conductor and tuned instruments.

Brain scans of people with DVD have revealed abnormalities in the basal ganglia, an group of neurons at the heart of the brain with several connections to other areas. Normal people show strong activation of FOXP2 here and fascinatingly, so do songbirds. Haesler reasoned that studying the role of this gene in birds could tell him more about its human counterpart.

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Doctors repress their responses to their patients’ pain

A new study shows that experienced doctors learn to control the part of their brain that allows them to empathise with a patient’s pain, and switch on another area that allows them to control their emotions.

Many patients would like their doctors to be more sensitive to their needs. That may be a reasonable request but at a neurological level, we should be glad of a certain amount of detachment.

In some doctors, being detached can be a good thing.Humans are programmed, quite literally, to feel each others’ pain. The neural circuit in our brains that registers pain also fires when we see someone else getting hurt; it’s why we automatically wince.

This empathy makes evolutionary sense – it teaches us to avoid potential dangers that our peers have helpfully pointed out to us. But it can be liability for people like doctors, who see pain on a daily basis and are sometimes forced to inflict it in order to help their patients.

Clearly, not all doctors are wincing wrecks, so they must develop some means of keeping this automatic response at bay. That’s exactly what Yawei Chang from Taipei City Hospital and Jean Decety from University of Chicago found when they compared the brains of 14 acupuncturists with at least 2 years of experience to control group of 14 people with none at all.

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Molecule’s constant efforts keep our memories intact

Our memories are more fragile than we thought. New research suggests that they need the constant action of a key protein to remain stored in our minds – block the protein and erase the memories.

Memories are dynamic things, unlike books stored on library shelves.Our mind often seems like a gigantic library, where memories are written on parchment and stored away on shelves. Once filed, they remain steadfast and inviolate over time, although some may eventually become dusty and forgotten.

Now, Reut Shema, Yadin Dudai and colleagues from the Weizmann Institute of Science have found evidence that challenges this analogy. According to their work, our memory is more like a dynamic machine – it requires a constant energy supply to work. Cut the power and memories are lost.

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Babies can tell apart different languages with visual cues alone

Most of us could easily distinguish between spoken English and French. But could you tell the difference between an English and a French speaker just by looking at the movements of their lips? It seems like a difficult task. But surprising new evidence suggest that babies can meet this challenge at just a few months of age.

The shapes of our mouths when we speak provide valuable clues that we can use to understand language.Young infants can certainly tell the difference between the sounds of different languages. Whitney Weikum and colleagues from the University of British Columbia decided to test their powers of visual discrimination.

They showed 36 English babies silent video clips of bilingual French-English speakers reading out the same sentence in one of the two languages. When they babies had become accustomed to these, Weikum showed them different clips of the same speakers reading out new sentences, some in English and some in French.

When the languages of the new sentences matched those of the old ones, the infants didn’t react unusually. But when the language was switched, they spent more time looking at the monitors. This is a classic test for child psychologists and it means that the infants saw something that drew their attention. They noticed the language change.

Weikum found that the babies have this ability at 4 and 6 months of age, but lose it by their eighth month. During the same time, other studies have found that infants become worse at telling apart consonant and vowel sounds from other languages, and even musical rhythms from other cultures.

Babies can distinguish between two languages from birth.It seems that initially, infants are sensitive to the properties of a wide range of languages. But without continuing exposure, their sensitivities soon narrow without continuing exposure to both languages, the babies’ sensitivities soon narrowed to the range that is most relevant for their mother tongue.

To test this idea, Weikum repeated his experiments on bilingual infants. Sure enough, at 8 months, these babies could still visually tell the difference between English and French speakers.

We normally think of lip-reading as a trick used only by deaf people. But this study suggests that the shapes our mouths make when we talk provide all of us with very important visual clues.

From a very early age, infants are programmed to sense these clues, and this so-called ‘visual speech’ may even help them to learn the characteristics of their native tongue.

Reference: Weikam, Vouloumanos, Navarra, Soto-Faraco, Sebastian-Galles & Werker. 2007. Visual language discrimination in infancy. Science 316: 1159.

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Experience tunes a part of the brain to the shapes of words

A new brain imaging study has found a part of the brain specifically attuned to the shape of written words. And unlike other similar areas, this one develops its abilities through learning and experience.

Over the course of evolution, certain parts of our brain have been specifically tuned to faces, human bodies and landscapes. These structures turn up in the same places in very different people. Their roles are so fundamental to the way we (and our ancestors) experience the world, that they have been long since hardwired into our genetic plans.

Words on the brain

Reading and writing are too new for evolution to have shaped our brains to them.But not everything we see is like this. Words, for example, are an exception. Even though reading and writing are such central parts of our lives now, they have only been around for a few millennia. And for most of that time, they were skills available only to a learned elite.

The entire history of writing is a mere blip in evolutionary time, certainly not long enough to evolve a specialised, genetically determined brain region dedicated to processing written words. Nonetheless, one such region exists.

Chris Baker and colleagues from the National Institute of Mental Health, Bethesda, have found that a small part of the brain specifically recognises written words. And unlike the areas that recognise faces and bodies, its origins lie in learning and experience.

Where words are recognised

Baker examined the brain activity of several English speakers using functional magnetic resonance imaging (fMRI), a technique that measures the flow of blood and oxygen in the brain. He found that a small region at the back of the brain – no bigger than a piece of sweet corn – responds strongly and specifically to English words.

The cLSSR only recognises Hebrew characters in Hebrew speakers.Strings of consonants worked just as well but strings of numbers or Hebrew words (right), which use unfamiliar characters, triggered much weaker responses. And the region responded even more weakly to line drawings of common objects or Chinese characters, which obviously perform the same function as English words but are very different in appearance.

Baker gave the region the slightly unwieldy name of ‘candidate letter string-selective region’ or cLSSR for short. He had its location, but it was still unclear if its properties are innate of the product of experience. Indeed, the cLSSR lies very close to the fusiform gyrus, a part of the brain genetically programmed to recognise faces and numbers.

Things got interesting when Baker repeated his experiments in people who were fluent speakers and readers of both Hebrew and English. Their cLSSRs responded equally strongly to both English and Hebrew words. But in all other ways, they behaved identically to the cLSSRs of those who just spoke English.

Nature and nurture

These results provide powerful evidence that experience shapes the abilities of this part of the brain. It’s obvious that experience breeds familiarity. But this is the first time that someone has shown that a part of the brain becomes specifically attuned to a type of visual through experience and learning alone.

The cLSSR is found in the extrastriate cortex in the back of the brain.Obviously, a genetic influence on the cLSSR cannot be ruled out. After all, genes control the structure of the developing brain, and in different people, the cLSSR is consistently found in the same place. This is most often in the left hemisphere. If it is damaged in adults, the right hemisphere can’t pick up the slack, and people suffer form problems in reading.

All this suggest that this particular bundle of neurons may develop its taste for words, but it is somehow predisposed to do so. Baker speculates that the cLSSR’s lies along the route that nervous signals take from visual areas to language areas, and gradually learns from the signals it carries.

The discovery of the cLSSR is just the beginning, and the questions practically ask themselves. Is it more diffuse or less responsive in dyslexic children? And how does it grow and develop over time? More research and new methods even more accurate than fMRI will help to provide the answers.

Reference: Baker, Liu, Wald, Kwong, Benner & Kanwisher. 2007. Visual word processing and experiential origins of functional selectivity in human extrastriate cortex. PNAS 104: 9087-9092.

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Drugs and stimulating environments reverse memory loss in brain-damaged mice

Scientists have restored lost memories in brain-damaged mice by giving them an experimental group of drugs, or by placing them in a stimulating environment. Their remaining neurons re-wired themselves and retrieved memories that had been misplaced, not lost, providing hope for treating human conditions like dementia and Alzheimer’s disease.

Dementia results in massive neuron loss, but that doesn’t mean memories are destroyed.You swallow the pill. As it works its way through your digestive system, it slowly releases its chemical payload, which travels through your bloodstream to your brain. A biochemical chain reaction begins. Old disused nerve cells spring into action and form new connections with each other. And amazingly, lost memories start to flood back.

The idea of a pill for memory loss sounds like pure science fiction. But scientists from the Massachussetts Institute for Technology have taken a first important step to making it a reality, at least for mice.

Andre Fischer and colleagues managed to restore lost memories of brain-damaged mice by using a group of drugs called HDAC inhibitors, or by simply putting them in interesting surroundings.

They used a special breed of mouse, engineered to duplicate the symptoms of brain diseases that afflict humans, such as Alzheimer’s. The mice go about their lives normally, but if they are given the drug doxycycline, their brains begin to atrophy.

The drug switches on a gene called p25 implicated in various neurodegenerative diseases, which triggers a massive loss of nerve cells. The affected become unable to learn simple tasks and lose long-term memories of tasks they had been trained in some weeks earlier.

A richer environment

Lost memories can be recovered by encouraging surviving neurons to re-wire themselves.Fischer moved some of the brain-damaged mice from their usual Spartan cages, to more interesting accommodation. Their new cages were small adventure playgrounds, replete with climbing frames, tunnels and running wheels, together with plentiful food and water.

In their new stimulating environments, the mice returned to their normal selves. Their ability to learn improved considerably, and amazingly, seemingly lost memories were resurrected.

They didn’t grow any new neurons, and their brains remained the same size. But Fischer found that they did have many more synapses – the connections between nerve cells – than brain-damaged peers. Even though they had lost a substantial number of neurons, their enriched environments triggered the surviving cells to re-wire themselves.

These experiments suggest that lost memories are in fact not lost at all, but misplaced. The dead neurons take important connections with them and the survivors, though incommunicado, still retain latent traces of memory.

When they are jolted into action and form new networks, these trace memories are reinstated. And that provides genuine hope for people affected by dementia, Alzheimer’s and other conditions.

Memory-restoring drugs

Brain damage from Alzheimer’s disease could potentially be reversed by HDAC inhibitors.It would be a touch silly to suggest putting such people in the equivalent of a large playpen. But Fischer also found a group of drugs called HDAC inhibitors that have the same effect – the molecular equivalent of a stimulating environment.

HDACs or histone deacetylases control whether genes are switched on or off by altering other proteins called histones. DNA winds around histones like spools, which serves to package this long and unwieldy molecule into a compact and more manageable form.

HDACs change the histones so that they wrap more tightly around DNA and render its genetic code unreadable. Any genes contained in these stretches of DNA are silenced. Drugs like sodium butyrate (SB) neutralise HDACs, freeing DNA from the repressive grip of histones.

Any silenced genes can now be freely switched on and among these, are genes that allow the brain’s neurons to sprout new synapses. The details still need to be ironed out, but the results are clear – just like mice housed in fun cages, those treated with SB regained lost memories.

The next steps

Naysayers might point out that these results are all very good for mice, but are a long way off benefiting people. But while our brains outclass those of mice, we appear to store memories in very similar ways. New experienced are initially encoded among the neurons of the hippocampus, only to be transferred into deeper and long-term stores about three or four weeks later.

Four years ago, a man who had been barely conscious for almost 20 years began to move and speak again. His nerves, badly damaged by a car crash, had started to re-wire themselves and form new connections, in the same way that Fischer’s rats did. The possibilities are there; it’s just the method that needs refinement.

At the moment, the biggest problem with Fischer’s approach is that it’s akin to shooting at a fly with a shotgun. HDAC inhibitors have far-reaching effects on a multitude of different genes. It’s fortunate that these include genes that lead to brain re-wiring, but such a scattershot approach is prone to collateral damage.

Documenting the full actions of HDAC inhibitors is vital. It will allow scientists to understand what side effects such treatments would have in people, while designing more sophisticated drugs with a narrower range of targets.

Reference: Fischer, Sananbenesi, Wang, Dobbin & Tsai. 2007. Recovery of learning and memory is associated with chromatin remodelling. Nature doi:10.1038/nature05772

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9/11 memories reveal how ‘flashbulb memories’ are made in the brain

Our memories of traumatic or shocking events are particularly vivid and carry strong emotional content. Now, a study of New Yorkers who witnessed the World Trade Centre attacks tells us how ‘flashbulb memories’ are formed.

I have only ever seen one car crash and I remember it with crystal clarity. I was driving home along a motorway and a car heading the opposite way simply veered into the central reservation. Its hood crumpled like so much paper, its back end lifted clear off the tarmac and it spun 180 degrees before crashing back down in a cloud of dust.

All of this happened within the space of a second, so the details may be different to what I remember. But the emotions I felt at the time are still vivid – the shock of the sight, the fear for the passengers, the confusion over what had happened.

Traumatic events like 9/11 produce a special type of memory. Many studies have shown that peoples’ memories become particularly clear when it comes to traumatic or shocking events.

Even learning about a shocking event, rather than witnessing it first-hand, can produce unusually clear recollections. Many of us still remember where we where when we learned that famous figures like Princess Diana or John F. Kennedy had died (I found out about Diana on the toilet).

Scientists have suggested that this type of event triggers a process that produces a very specific and exceptionally vivid type of memory called a ‘flashbulb memory’. This concept has been kicking around since the 1970s, but the evidence that flashbulb memories actually exist is inconsistent.

Tali Sharot and colleagues form New York University decided to find some proper answers by studying the brain activity of people remembering a traumatic event.

Doing such experiments would normally be ethically impossible – you cannot after all willingly traumatise someone in the name of science. But Sharot did not need to – unfortunately for us, the twenty-first century has already provided its fair share of traumas.

On September 11, 2001, the people of New York experienced terror and devastation on a massive scale. If any event led to the formation of flashbulb memories, this one would.

Sharot recruited 24 people who had witnessed the World Trade Centre attacks first-hand and asked them to remember either the attacks, or a random event from another summer.

She found that people who were in Downtown Manhattan near the attacks had distinctly different memories than those who were twice as far away in Midtown.

The Midtown group recalled their 9/11 memories in the same way as their generic ones. But the Downtown group remembered their 9/11 experiences more vividly, strongly and confidently and gave both longer and more detailed descriptions. They reported seeing the towers “burning in red flames”, smelling the smoke and hearing “the cries of people”.

The amygdala is the brain's emotional control centre. Not content with relying on descriptions. She hooked the witnesses up to a brain scanner to she if these differences were mirrored in their brains – specifically, in a small region called the amygdala, the brain’s emotional control centre. The amygdala affects how memories are stored in the long-term and animal studies have shown that this storage is influenced by stress hormones.

Sure enough, when asked them to think about 9/11, the Downtown group showed much greater activity in their left amygdala, while the Midtown group did not.

Despite these results, Sharot is still tentative about concluding that flashbulb memories, as they are classically defined, exist.

Nonetheless, her results clearly show that experiencing a shocking event yields a very different and exceptionally vivid type of memory than the humdrum occurrences of daily life. These memories – flashbulb or not – are formed through a special mental route which involves the amygdala.

And Sharot’s brain scans turned up something more unexpected. When the Downtown group thought about 9/11, they also showed much lower activity than normal in the parahippocampal cortex.

This part of the brain is thought to be involved in processing and recognising details of a scene or event. If its neurons are dimmed during shocking situations, this could explain why people who experience surprising events remember how they felt, but cannot reliably provide details.

During the tragic shooting of Jean Charles de Meneses last year, eyewitnesses proved to be wildly inaccurate, with first-hand accounts of his clothing, police action, and the number of shots fired clearly contradicting each other. If emotions are prized over details in memories of shocking events, how much value can we truly place on eyewitness accounts?

Sharot, Martorella, Delgado & Phelps. 2006. PNAS 104: 389-394.

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Asymmetrical brains help us (and fish) to multi-task

The asymmetry of the human brain may allow us to cope with multiple demands that compete for our attention. The link between brain asymmetry and multi-tasking has now been confirmed in experiments with artificially-bred fish.

As you read this article on the internet, your computer is busy. You may be running multiple programs in the background, with email clients, anti-virus software or file sharing software all competing for valuable memory. The ability of computers to multi-task has grown substantially in recent years, as processors have become increasingly powerful.

Evolution has chartered a similar course, and humans have a particularly strong talent for dividing our attention among multiple priorities. Now scientists are showing that the asymmetrical differences between the two sides of our brain are essential for this ability to multi-task.

In the animal world, the ability to multi-task is a matter of life and death. Many species must be ever-watchful for food, while simultaneously looking out for predators who would view them in the same way.

Like too many open applications that slow down a computer, these multiple tasks compete for the brain’s finite resources. Those who survive life’s challenges are those with an edge at efficiently dealing with multiple demands.

The human brain - not symmetricalOne way of doing this is to use parallel processing – to delegate different parts of a problem to different pieces of hardware.

This is exactly the situation found in the human brain, with two asymmetric hemispheres associated with different mental abilities. And this ‘lateralisation’ is not unique to us, but seems to be present in all back-boned animals, from fish to apes.

An explanation for this asymmetry now becomes obvious – it may allow animals to multi-task, acting as a sort of cerebral division of labour.

(Un)evenly-brained fish

Marco Dadda and Angelo Bisazza at the University of Padova decided to test this idea, by looking at small freshwater fish called killifish. They bred different strains of this species with either symmetrical brains or asymmetric ‘lateralised’ ones.

The fish were kept in a special tank consisting of two parts separated by a trap door. In one half – the ‘feeding zone’ – the researchers placed a live brine shrimp for the fish to eat.

A killifishBoth strains were equally adept at catching the shrimp, but the lateralised strain gained a massive advantage when a predator was brought into play.

Dadda and Bisazza occasionally placed a tank containing the larger predator pumpkinseed sunfish in front of the feeding area, so that any killifish swimming across found itself face-to-face with a threat. When this happened, the symmetrically-minded ones took twice as long to catch their meals, but their lateralised peers took barely a second longer.

When the fish had to divide their attention between watching the predator and catching the shrimp, the lateralised brains acted as parallel processors, allowing them to cope with both tasks simultaneously.

Dadda and Bisazza confirmed this interpretation by carefully watching the fish as they swam after their meals. Killifish catch their food by approaching from the side, using one eye to monitor the prey.

In the absence of the sunfish, they were equally to strike from either side. But with the predator around, in 7 out of 10 times they snapped at the shrimp on the same side, watching it with one eye, and the predator with the other.

The pros and cons of asymmetry

In the case of the killifish in this experiment, partitioning roles to different parts of the brain seems to have brought clear benefits. But Dadda and Bisazza are quick to point out that the situation in the wild is less obvious.

In many cases, species with lateralised brains show lateralised behaviours, preferring to turn, keep watch or catch prey on one side of their body. Their other side is less often guarded, and natural selection penalises them for it by producing predators that prefer to approach from the unguarded side.

In these cases, regardless of parallel processing power, an asymmetric brain is clearly a disadvantage. The two scientists believe that the tipping point between these pros and cons comes when an animal has to perform difficult mental tasks.

Other studies have shown that asymmetrical brains endow wild chimpanzees with superior termite-fishing skills, and (equally wild) human children with better mathematical and verbal abilities than their classmates.

It may be that over the course of evolution, our brain’s halves started to work together more effectively as they became more different and specialised. It is ironic and sad then, that the opposite seems to hold true for the divergence of human cultures.

Dadda & Bisazza. 2006. Animal Behaviour 72: 523-529.