The Broken Escalator Effect (It’s Real)

Posted on June 19, 2013 by | 8 comments

Every day we take the Paris Metro and RER to and from class. It’s a relatively painless trip, except when there’s a strike going on (which has been almost every day). One day last week, as our motley crew filed through our favorite station, Châtelet, to transfer trains, we reached our favorite stretch of the station: the moving walkways. I approached the walkway without hesitation, took a step onto the belt, and immediately felt myself jolted awake by a sense of falling. As it turned out, the moving walkway was broken that day, and pedestrians were just using it as a normal path. I followed suit and laughed silently at how funny I must have looked to anybody who saw me nearly fall on my face.

Our favorite Metro stop

Later that afternoon, on the return journey, I’d had ample time to wake up during the day. As we approached the same collection of moving walkways, I made sure to take note of the functionality of the machines. They were all still broken, but I decided to follow the crowd and walk along one of the belts anyway. This time, I approached, took a step, and felt jolted again! I was shocked at my brain’s miscalculation despite my conscious awareness that the walkway was stationary. I presumed that it had to be some sort of perceptual memory that I had for moving walkways. Perhaps because reality wasn’t matching up with what my brain had learned to be true of “people-movers” countless times before, my mind was having trouble adjusting. I decided it was worth a search in the literature when I got home.

No "broken escalator effect" here

What I found was not only reassuring for my vestibular system, but also immensely interesting. There is an extensive collection of scientific research on what has been called the “broken escalator phenomenon,” (Reynolds and Bronstein, 2003). Evidently, the effect is more evident on moving walkways, but because nobody knows what to call them, the original authors of the phrase decided to go with escalator instead. Once the phenomenon became well known as a common occurrence in city-dwellers, researchers sought to describe what was actually happening to cause this “feeling of uneasiness” despite absolute consciousness of the fact that the conveyor was not moving

First, experimenters had subjects walk on a short, stationary moving walkway a few times while measuring walking speed, postural sway, and muscle contraction (Reynolds and Bronstein, 2003). Afterwards, the experimenters turned on the walkway and had the same subjects board the machine. Not surprisingly, subjects made several physical changes as they got used to the moving version, but the most significant change observed was in the actual velocity of movement just prior to boarding. Naturally, the subjects increased their pace by .3 m/s in order to minimize being jerked by the belt. This is similar to what happens to us in everyday life. We encounter a majority of moving walkways in their “on” position, and we become accustomed to increasing pace, leaning forward, and flexing our leg muscles as we approach them. Next, the researchers informed the subjects that the walkway would be turned off, and in fact, they could see so for themselves. When they approached the walkway this time, all subjects stumbled, and many were shocked or laughed at the occurrence. Analysis of the physiological data showed that approach velocity, trunk lean, and muscle contraction took place at levels in between normal walking values and the values seen when subjects were accustomed to the moving walkway. It seemed that the brain was confused by seeing a normally moving pathway in a motionless state, and addressed the situation by “hedging its bets” so to speak. Interestingly, repeating a second trial with the “off” walkway shows no signs of distress. The brain learns quickly to adopt normal walking motor programs for the motionless walkway. Further studies have shown that skin conductance also increases just prior to experiencing the “broken escalator phenomenon,” implying that subconscious, fear-based mechanisms are at play (Green et al., 2010). This may explain why the hiccup occurs even when one consciously recognizes that normal walking will suffice.

Primary motor cortex, where the researchers stimulated.

Given that this phenomenon is strikingly similar to the lack of balance that many neurological disease patients experience, further studies aimed to find ways to modulate to the occurrence (Kaski et al., 2012). Recently, researchers tried this using a technique called transcranial direct current stimulation (tDCS), which is a lot like connecting a battery to your skull, except it’s scientific. Subjects went through the same experimental procedure as in the first study, but just before had a small anodal current passed through their brain for 15 minutes before the moving platform phase of testing. The researchers targeted the primary motor cortex, an area of the brain responsible for executing movement and storing motor memories, or the actual plans that the body uses to coordinate movement. The researchers believed that the broken escalator effect occurred due to an inability to suppress the brain’s default “moving walkway motor plan,” so activating primary motor cortex would cause the phenomenon to become even more extreme. Indeed, the subjects who received the electrical stimulation showed a larger broken escalator effect and took more trials to adjust to the stationary pathway than control subjects who received no stimulation. Though the nature of the experiment did not necessarily prove that the broken escalator effect is due to overactive motor memory, the results are significant in that they show it is possible to manipulate gait and motor problems with relatively simple technology. tDCS is fairly cheap and straightforward compared to other similar technologies, and its lack of precision actually lends itself nicely to working with the distributed neural systems of locomotion. Though this study used tDCS to worsen a locomotor problem, this same system may soon become a useful tool in neurological diseases that show locomotor symptoms such as stroke, Parkinson’s multiple sclerosis, and Alzheimer’s disease.

 

-Max Farina

 

References:

Reynolds RF, Bronstein AM (2003) The broken escalator phenomenon. Experimental Brain Research.

Green DA, Bunday KL, Bowen J, Carter T, Bronstein AM (2010) What does autonomic arousal tell us about locomotor learning? Neuroscience 170: 42-53.

Kaski D, Quadir S, Patel M, Yousif N, Bronstein AM (2012) Enhanced locomotor adaptation aftereffect in the “broken escalator” phenomenon using anodal tDCS. Journal of Neurophysiology 107: 2493-2505.

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Pay Attention, Brain

Posted on June 19, 2013 by | 6 comments

It’s 9:30 in the morning and I’m sitting in class listening to this old geezer talk about neuroscience. This is even more disheartening since I am in Paris over the summer break. As we touch upon genetic engineering, my mind takes this weird but quick neuronal pathway from genetic engineering to genes then jeans and finally shopping at the Avenue des Champs-Elysees. What a great time that was. We stopped by the Laduree and picked up some of the best macaroons in Paris. As I was falling deeper into the pleasures of my mind, I hear arguments over ethical reasons against pre-implantation genetic diagnosis from the other neuroscience students which quickly snaps me back to reality. I try to refocus my attention to the discussion at hand so I can put my two cents in for the day. As much as I love talking about enhancing the human race, my mind has the tendency to wander the streets of Paris.


The blue is the Accent center where my class is. The red is where my mind is, avenue des Champs-Elysees.

When my mind wanders, it isn’t a conscious choice (at least for the most part). It feels like sudden jolt of random associations till I get a sustained daydream or I realize I am wandering and stop. The default network is the culprit here. It is a network of brain regions that is known to become active during wakeful rest which is associated with mind wandering. In a default network study, subjects were trained to meditate by focusing on their breathing. They were then placed into an fMRI machine that measures brain activity via changes in blood flow. As soon as the subjects noticed their mind wandering away, they pressed a button and drew their attention back to their breathing. During the wandering stage, the fMRI revealed activity in the default network such as the posterior cingulate cortex (PCC), which is known to integrate all sorts of sensory information. Another part of the default network is the medial prefrontal cortex (mPFC) which is known to attribute mental states such as desires to oneself and others (theory of the mind) (Hasenkamp et al., 2012). As the subjects drew attention back to their breaths, the default network shuts off and a cluster in the dorsolateral prefrontal region remains active. This region is responsible for high cognitive processes such as organization, planning, etc…. It makes sense that your dorsolateral prefrontal region turns off when your mind wanders since there is no need for the higher processes when you’re not actively thinking.

Thus during the first 10 minutes of every morning lecture, my dorsolateral prefrontal cortex is highly active and maintained. Then, perhaps due to fatigue or boredom, my dorsolateral prefrontal activity starts to wane and my default network kicks in. I am now suddenly at the top of the Eiffel tower, taking in the beautiful scenery. At some point I realize I’m in class and my dorsolateral prefrontal cortex reactivates and my default network becomes quiet again. Whether the activity of the default network causes one to wander or vice versa is unknown. However I personally believe that the over activation of my default network is what causes me to lose crucial participation points in my class.

~James Eun

Hasenkamp W, Wilson-Mendenhall CD, Duncan E, Barsalou LW (2012) Mind wandering and attention during focused meditation: a fine-grained temporal analysis of fluctuating cognitive states. NeuroImage 59:750-760.

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How Can You Tell I’m American?

Posted on June 19, 2013 by | 7 comments

One of the greatest challenges about being in Paris is being constantly exposed to a foreign language. I have found that fewer Parisians than expected speak English. Having studied French for a number of years, I am always eager to test my ability to communicate with native French speakers. I try to practice French in Paris as often as possible, whether it is through ordering food (obviously my most important application of the language), asking for directions, or even giving directions sometimes. Just a couple of days ago I asked a young lady for directions while on the metro and even though I knew that I had appropriately phrased my sentence in French, she responded in English. I knew that my accent had given away the fact that my native language is English, but I had expected her to respond in French. I have found myself in similar situations on many occasions. One time I was speaking French to an angry Cite Universitaire, the campus on which we are living, security guard after I had been locked out of my room and he responded in English, “I don’t speak English.” I was puzzled and in French let him know that I can speak French and he responded, “no you can’t.” I chose not to take this second encounter personally and instead began to wonder what about my speaking bothered him so much. It must have been my accent. Accent perception is such an interesting concept. We can tell what country a person is from, or even perhaps the city in which they were born not by listening to the words that they say, but by listening to the way that they say them.

Cite Universitaire (labeled as A)- where we have been living for the past 3 weeks.

In a study done by Adank et al. (2011), native monolingual Dutch speakers were played Dutch phrases in a Dutch accent and were also played the same Dutch phrases in an unfamiliar accent. While listening, the subjects’ brains were monitored using an fMRI scanner, a machine which uses magnetic imagining to monitor brain activity. The study showed that when the sound stimuli changed from the familiar to the unfamiliar accent, more of the subjects’ superior temporal gyrus (STG), a brain area involved in basic auditory language processing, became activated. The STG has also been shown to be associated with phonetic-analytic listening to speech. Perhaps this gives insight into as to why more of the STG is activated when listening to an unfamiliar accent; the brain is recruiting more cells to help analyze the phonetics of the speech because the speech is foreign. It is important to understand this because when French individuals hear me speaking French with an English accent, their STG becomes increasingly activated and they recognize that not only am I speaking in an accent, but then, through using other areas of the brain, may be able to understand what language I am speaking.

An exhibit in the Louvre Museum spelling out "love differences" in many different languages.

Whenever I’m on the metro and everyone around me is speaking French, it is difficult for me to decipher what they are saying unless they are speaking directly to me. I was curious as to the ways in which my brain would have responded to the sounds on the metro had I learned French at a younger age, but second to English. I wondered how the bilingual brain responds to language perception in general. In a study done by Archila-Suerte et al. (2012), a group of bilingual Spanish-English speaking children (whose native language is Spanish) and monolingual English speaking children were played the English syllables, “saf,” “sof,” and “suf,” while watching a silent film. These syllables were chosen because they are pronounced similarly in Spanish and would provide more insight into activation of the bilingual brain (perhaps because they may activate regions involved in perception of both languages). The subjects were told to focus on the silent film while the syllables were being played to them and simultaneously the group was analyzing the subjects’ brains using an fMRI scanner. The study was performed for young and older bilingual and monolingual children. The group found that the young monolingual and bilingual children had the STG activated (let’s call this area 1) while listening to the syllables. This data implies that the bilingual children when just beginning to learn the second language perhaps relates it to the first language and processes it in the same brain area. However, the older monolingual children still only had area 1 activated during the task whereas bilingual children had area 1 as well as other areas in the brain activated. This suggests that as bilingual children begin to master a second language more, their brain recruits other areas, other than area 1, to help distinguish between the two languages. Perhaps my brain is similar to the brain of the younger bilingual children, since I have not yet begun to master the French language. My brain may not be able to recruit other areas to help area 1 decipher a language other than English and this may be why I am unable to easily pick out French words and conversations while on the train. However, French individuals who are able to easily recognize my accent, process what my native language is, and then respond in my native language perhaps have activation of other brain areas which help the STG decipher the language. This is due to the idea that they are bilingual and no longer need to relate their second mastered language to their native language. It would be interesting to see what the combined results of the first and second study would be; to pursue a study that looked at monolingual and bilingual individuals’ brain activation to speaking their common language in an accent. I am curious to see if by being well versed in more than one language, bilingual children are able to recognize accents easier. Maybe one day I’ll master the French language enough to not have to constantly compare it to English! I guess I’ll just have to ensure that this isn’t my last trip to Paris…

–          Ankita Gumaste

Adank P, Noordzij ML, Hagoort P (2011) The role of planum temporal in processing accent variation in spoken language comprehension. Human brain mapping 33: 360-372.

Archila-Suerte P, Zevin J, Ramos AI, Hernandez AE (2012) The neural bases of non-native speech perception in bilingual children. NeuroImage 67: 51-63.

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Enter the Abyss

Posted on June 19, 2013 by | 3 comments

Let’s take a little adventure into the dark unknown. You pass through a doorway on the streets of Paris and see a tiny spiral staircase up ahead. The steps hold no more than one person, and are smoothed over and slippery. You make your way down, ever wondering when the dizzying staircase will end. Finally you stumble into a long, dim hallway. The air is moist, and water drips from the ceiling forming dirty, shallow puddles on the stone. You can see into the tunnel, but not where it ends. The eerie yellow light is your only guide into the deep.

The hallways stretch on and on, twisting and turning until you’ve lost all sense of direction, as you cling to the path that will bring you to safety. Suddenly, you enter a larger room with round, stony pillars, and a doorway straight ahead. The sign above the door reads “Stop. This is the Empire of the Dead.” At last, you enter the infamous repository of 6 million people across French history, the Catacombs.

As a child, I loved watching and reading about spooky things. From my first taste of the supernatural watching “Goosebumps” and “Are You Afraid of the Dark?” on television, I developed a complicated interest in all things scary. Though I could only watch these shows in broad daylight and would have nightmares about them at night, still I wished to see how the stories would unfold for the unsuspecting characters in every plotline. Eventually I stumbled onto the Catacombs, which surprisingly was one of the first things I learned about Paris (apart from the Eiffel Tower of course). The Catacombs are the resting place for French civilians when the cemeteries became overcrowded. Rather than finding land elsewhere, the bones of already interred people were shoved deep underground, in an abandoned mine. The depressing history and unsettling feeling of displeased spirits in the Catacombs was more than enough to convince me to visit, if I can muster up the courage that is.

Map to help locate the Catacombs

 

When I entered the Empire of the Dead, my brain was already on full alert. Dark, suffocating passageways deep underground are enough to send my brain into overdrive, but the thought of crossing paths with millions of skeletons added another element of fear. When I laid eyes on the first wall of bones, I had a mild panic attack. Internally of course, I couldn’t show the rest of the group the fear. Still, the sight was beyond creepy, on so many levels.

Every side of the wall was covered in rows upon rows of human bones, with skulls laid halfway up and at the very top of the walls. It wasn’t so much the bones themselves as the thought that someone physically did this. Someone separated the bones of a skeleton from each other, and created the walls out of human remains. I wonder what those spirits would say, if they were to say anything at all.

These pictures don’t do justice to the atmosphere of the dark, gloomy corridors, filled with the bones of people of long ago.

As I climbed up another dizzying spiral staircase and took a lungful of fresh air, I began to see just how silly my fear of the catacombs were. In all reality, it wasn’t that scary. However, I anticipated a scary scene, and so my fear mode was already fully engaged by the time I actually saw the skulls and bones. What caused this anticipated fear-event fear response, so to speak? I found my answer when I began reading an article about different versions of a gene that can cause an enhanced fear and anxiety responses (Glotzbach-Schoon et al., 2013). Reading the experiment has helped me understand why I reacted the way I did, learning something a little more about my brain and fear responses in general.

This study examined the role of variants of 2 genes, 5HTT  and NPSR1. Previous research has shown that the 5HTT gene is involved in anxiety disorders, while the NPSR1 gene has an important role in anxiety and fear responses. The researchers studied two forms of each gene, entitled either S+ or LL for the 5HTT gene and T+ or AA for the NPSR1 gene. The patients had a combination of each copy, with 4 different combinations in total. They used a virtual reality simulator to test for fear conditioning (developing a fear for something). When conditioning the fear response, patients in one virtual office room were given an unpredictable, mildly painful electric shock. Those in another virtual office room did not have the same electric stimulus. The researchers examined fear and anxiety responses with the behavioral technique fear conditioned startle reflex, which studies the increase in startle response when in the fear state. They measured the startle response with Eyeblink Electromyogram (EMG), a fancy name for tool to measure eye blinking.

Results of the study indicate that patients who had both S+ and T+ variants of the genes exhibited a higher startle response when in the electric shock office room. However, patients that had the AA variant regardless of the forms for the 5HTT gene were more anxious in the experiments. The results are interesting because they not only show that different forms of the same gene can influence our behavior, but also they demonstrate possible gene interaction for the startle response, whereas only one form of the gene affects anxiety.

Maybe I have the double S+/T+ combo because I had a higher startle response when seeing the bones than I had expected. Or maybe I just have the AA gene and was more anxious to see the human remains when entering the deep. In either case, though I knew what was coming at the end of the long, dark tunnels, still I couldn’t control my fear when I finally entered the Empire of the Dead. Despite my weird love for the fear state, I don’t think I will disturb these bones again–the Catacombs is one place that I wouldn’t mind skipping on my return to Paris. At least I can cross this frightful experience off of my bucket list. Check mark.

-Mayur Patel

 

Reference:

Glotzbach-Schoon E, Andreatta M, Reif A, Ewald H, Troger C, Baumann C, Deckert J, Muhlberger A, Pauli P (2013) Contextual fear conditioning in virtual reality is affected by 5HTTLPR and NPSRI polymorphisms: effects on fear-potentiated startle. Frontiers in Behavioral Neuroscience 7:31

Creative Commons map image:

http://images.travelpod.com/cache/accom_maps/Hotel-Du-Midi-Paris-Montparnasse.thumb.gif

 

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Poisoning Pigeons in the Park

Posted on June 18, 2013 by | 3 comments

We’ve now been in Paris for close to three weeks. It’s a wonderful city, and I’ve enjoyed so many terrific experiences since we arrived: long, sunny walks along the Seine from the Louvre Museum to the Eiffel Tower, terrific concerts by countless street musicians, and many delicious French crepes and baguettes! However, there’s one part of Paris that is slowly pecking away at my enjoyment of the city – Pigeons. 

Paris isn’t quite as famous for its pigeons as other large cities like New York and London, but their presence is certainly noticeable – especially if you attempt, as I did, to eat a fresh baguette under the statue of Charlemagne at Notre Dame, an area where the pigeon density rivals that of the tourists. As soon my first breadcrumb dropped, I was surrounded and bombarded by more birds than I could count. This happened again at Tuileries Garden, and yet another time on the Cite Universitaire campus.

Even when I’m not eating baguettes the pigeons seek me out. While relaxing in a small urban park near the Bastille I was lucky enough to receive a pigeon “deposit” on my pant’s leg, followed by another on my chest and a third that landed on my shoulder, narrowly missing my right ear. I can see one such gift being an accident, but three in a row makes me think that these pigeons might have a vendetta against me for the bird research I do back at Emory.

It turns out that I’m not the only one who’s annoyed with Paris’s bird problem. For many years the city has pigeon-proofed historical buildings by placing spikes on all the ledges where the birds might land. Additionally, in 2008 Paris officials set out to curb the pigeon population by building nesting-lofts throughout the city and then sterilizing the eggs while the birds were out feeding (bloomberg). Given my recent experiences, these attempts don’t appear to be working and so I looked into another possible method of population control – feeding the birds poison-laced food.

I was curious about how effective poisoning would be. Do the birds learn to avoid dangerous food? And if so, how quickly does this avoidance behavior develop, especially if that food had a distinct taste or smell associated with it?

How quickly do pigeons learn to avoid poison?

A map of the places I've had run-in with pigeons


In 1999 a study published in the Archives of Environmental Contamination and Toxicology looked exactly at how quickly pigeons learn to avoid poisonous-food and the effect of hunger on the amount of toxic food they ingested (Pascual et al., 1999).

The study used four groups of eight pigeons. Two of these groups were given as much food as they wanted (ad libitum) for the 6 days leading up to testing while the other two groups were deprived of food. The researchers did two experiments. First they offered seeds laced with the sulfurous-smelling toxin fonofos to one of the ad libitum groups and one of the deprived groups for 6 straight hours. The birds were videotaped throughout the test, and eating behavior was measured by the amount of food eaten as well as the rate at which it was consumed. The second experiment, using the remaining two bird groups, was very similar but the food was offered first for 2 hours followed by a half-hour break, and then for an additional four hours. While not much different then the first experiment, this test showed whether the birds were able to remember that the food was dangerous when exposed to it a second time.

On average, it only took the birds 6 minutes to learn to avoid the food and all of the pigeons from experiment two still avoided the food after a half-hour break. Five of the birds from the food-deprived group did die and the authors attributed this to the fact that these birds ate huge amounts of food in the first six minutes. This is interesting because it suggests that the ability to develop avoidance behaviors is dependent on time, not on the amount of food eaten. Additionally, the video recordings showed reactions (head shaking, food-spitting, vomiting) during the first six minutes, which confirmed that the food was unpleasant to the birds. Given the size of the Parisian pigeons that have harassed me so far, I doubt any of them are food deprived, so unfortunately poisons (or at least poisons that have odor or taste like fonofos) would not be effective.

While this article clearly documented the development of avoidance behaviors and specifically showed that internal state (such as hungry/not hungry) did not affect the rate at which these behaviors we were created, it did not discuss how these behaviors are mediated in the brain.

How is avoidance mediated in the brain?

A pigeon posing in front of the Eiffel Tower. A perfect summary of my experiences so far in France.

 

 

Most research in avoidance behavior concentrates on the role of a small almond-shaped region in the bottom-middle of the brain called the amygdala, which is thought to mediate avoidance behavior development (Davis, 1992). How exactly it does this is still being debated but the majority of articles suggest that the amygdala helps consolidate a memory associated with an unpleasant experience like eating food that makes you feel sick (Smith et al., 2001). More specifically, some research has shown that it plays a role in the initial acquisition of the memory (Wiliskey et al., 2005). Even though these studies were not done in pigeons, we can use can use them to predict what might have occurred in the pigeon experiment. When the pigeons first ate the fonofos food and experienced the unpleasant side effects, it’s possible that their amygdalae were activated and that a connection between the food and the effects was formed. However, this connection in the brain probably was not strong enough to cause avoidance after just one exposure to the food, so it took multiple exposures over the course of six minutes. Even though the food-deprived pigeons ate more, it’s possible that they didn’t avoid the food any faster than the ad libitum group because their hunger took priority and inhibited the avoidance behaviors from forming (Gilette et al., 1999).

Unless the Parisian pigeons have faulty amygdalae, which I highly doubt, I will unfortunately have to come up with another way to control their population. Perhaps, a poison that doesn’t have any smell or immediate unpleasant effects associated with it? Or maybe the best option is just to take all of my baguette eating indoors. Regardless, it does not appear that I will be poisoning Parisian pigeons anytime in the near future. Now that you’ve finished the post I recommend that you click on the following link and enjoy a 3 minute tune by 1960s comedian Tom Leher, it applies nicely.

http://www.youtube.com/watch?v=yhuMLpdnOjY

 

– Camden MacDowell

UPDATE: I GOT EVEN WITH THE PIGEONS!

mmm... tasty pigeon lunch! Literally the taste of revenge!

 

Works cited:

Davis M. (1992) The role of the amygdala in fear and anxiety. Annual Review Neursci 15:353-375

Gillete R., Hatcher N., Huang R., Moroz L. (1999). Cost-benefit analysis potential in feeding behavior of a predatory snail by integration of hunger, taste, and pain. PNAS 97: 3585-3590

Pascual J., Fryday S., Hart A. (1999) Effects of Food Restriction on Food Avoidance and Risk of Acute Poisoning of Captive Feral Pigeons from Fonofos-Treated Seeds. Arch. Environ. Contam. Toxicol. 37: 115-124

Smith DM., Freeman JH., Gabriel M., Monteverde J., Schwartz E. (2001) Lesions in the central nucleus of the amygdala: discriminative avoidance learning, discriminative approach learning, and cingulothalamic training-induced neuronal activity. Neurobiol Learn Mem 76: 403-25

Wilensky A., LeDoux J., Schafe G. (2005) Amygdala Modulates Memory Consolidation of Fear-Motivated Inhibitory Avoidance Learning But Not Classical Fear Conditioning. The Journal of Neurosci 20: 7059-7066

 

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Musée du Parfum & Synesthesia

Posted on June 18, 2013 by | 1 comment

This afternoon we went to the museum of perfume near the Paris opera house off Metro 8.  The museum is opened by a perfumery called Fragonard Parfumeur.  Fragonard Parfumeur was established shortly after WWI by an entrepreneur named Eugene Fuchs in 1926.  During the tour, we learned about different concentrations of perfume, their making techniques as well as the correct way to put perfume on yourself.  For example, Eau de Toilette is around 10% aromatic compound while the actual perfume is 20%.  Towards the end of the tour, we were given strips of paper scented with different perfumes.  One particular perfume named “Juste un baiser” or “Just a kiss” smelled sweet.  The perfume almost smelled like strawberry and mandarin orange dipped in honey.

Map of the Museum of Perfume

It is interesting how people often use adjectives for taste, or even food items to describe a smell.  We don’t hear people say this flower smells red, or this perfume smells loud.  This must indicate that there are some sort of overlap of brain processing for taste and smell.  This phenomenon is called “synesthesia” in which the stimulation of a sensory pathway leads to involuntary activation of a separate sensory pathway.  There are many different types of synesthesia that are not common to the majority of us.  For example, people with color-graphemic synesthesia view letters and numbers with a specific color (Rich and Mattingley, 2002), and people with number-form synesthesia view numbers in a specific location in space (Sagiv et al., 2006).  Therefore, odor-induced taste might be a universal form of synesthesia that most of us have experienced.

Different types of perfume

If odor-induced tastes are so similar to taste itself that people describe an odor “sweet”, then these odors are probably processed in the same area of the brain as tastes.  Not surprisingly, there are already multiple papers suggesting that the insula, part of the primary gustatory cortex that is responsible for the initial processing of gustatory signals, is also activated by odors that are able to induce taste-like sensations (Stevenson and Miller, 2013).  Instead of looking at the primary taste cortex, Stevenson and Miller (2013) investigated the two secondary gustatory processing areas of the brain: the orbitofrontal cortex (OFC) and the amygdala to see whether odors that induces tastes-like sensation are also processed through similar areas of the brain.  To test their hypothesis, they put 9 patients with brain resections in the anteromedial temporal lobe (AMTL) that included the amygdala, 3 patients with OFC damage, and 42 healthy controls through a series of gustatory and olfactory tests.  All test subjects were presented with 2 sweet-smelling odors (chocolate and plum) and 2 non-sweet-smelling odors (Vegemite and oregano).  An “odor-taste quality score” was based on the test subjects’ ratings of whether a smell is sweet, sour, salty, or bitter compared to the expected taste of the odor (Stevenson and Miller, 2013).  The result of this study shows that AMTL patients, while impaired in gustatory senses, were unimpaired in odor-induced taste tests.  On the other hand, one of the three OFC patients who was severely impaired in gustatory senses, was also impaired in odor-induced taste tests.  The data indicates that one of the two secondary gustatory processing areas, the OFC, is involved in both the processing of tastes, and odor-induced tastes.  Stevenson and Miller (2013) further showed that OFC and insula both have the same type of cells that are more responsible for the discrimination of tastes while the amygdala has cells that supports the recognition of tastes.  This is probably why both the insula and the OFC are needed for the processing of odor-induced tastes while the amygdala is not.

Red part shows the amygdala.

Green part shows the Orbitofrontal cortex (OFC)

This study shows that odor-induced taste is a type of synesthesia that is experienced by the majority of us, which also explains why we often use gustatory adjectives to describe a smell.  However, I think further research is needed to prove this concept because of the low sample size and the fact that only 1 out of 3 OFC patients showed correlation between impairment of taste and odor-induced taste.  In addition, there might be other unknown brain-related problems in these patients, which will affect the interpretation of the data.  Furthermore, an fMRI study of the areas of the brain are active during odor-induced taste tests could potentially provide a more accurate indicator for the overlap of brain processing area of taste and odor-induced taste.  Aside from all the potential flaws of the study, at least now we know that there are biological evidences behind all the taste and food-related description of different kinds of perfume!

-Eric Yao

References:

Rich AN, Mattingley JB (2002) Anomalous perception in synaesthesia: a cognitive neuroscience perspective. Nature reviews Neuroscience 3:43-52.

Sagiv N, Simner J, Collins J, Butterworth B, Ward J (2006) What is the relationship between synaesthesia and visuo-spatial number forms? Cognition 101:114-128.

Stevenson RJ, Miller LA (2013) Taste and odour-induced taste perception following unilateral lesions to the anteromedial temporal lobe and the orbitofrontal cortex. Cognitive neuropsychology 30:41-57.

 

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Paris, the City of Love

Posted on June 18, 2013 by | 3 comments

Visiting the Pont de Arts bridge in front of the Institut de France in Paris will leave you with a sense of true French “amour.” On father’s day, I had the opportunity to see the bridge up close. Despite seeing plenty of couples taking wedding pictures in front of the Eiffel Tower, buying macaroons at Laduree on the Avenue des Champs-Élysées, and enjoying an afternoon together in the gardens at the Palace of Versailles, the romance of this city hadn’t quite hit me. The instant I walked on to this bridge, I didn’t even notice the gorgeous view because I couldn’t see anything past the chain-linked railings on either side. I think I’m just starting to understand why Paris is known as the city of love.

Looking at the Institut de France from the Pont de Arts bridge

Looking at the Institut de France from the Pont de Arts bridge

On either side of the bridge, you will see thousands of locks that have been secured to the railings. The locks are on every grate all the way up from the bridge planks to the top of the fence. From a distance, the sides of the bridge appear to be completely opaque. I was actually worried that there might not be room to put more locks somewhere along the grates overlooking the Seine. To make sure the love that the lock represents lasts forever, the tradition is to throw the keys over the bridge and into the river after you secure the lock to the bridge. While this may be an act of littering, I guess the French disregard it for the sake of romance.

While plenty of couples do this to ensure their relationship will last forever, plenty of people do it for their families as well. As a girl who has grown up in a big family, I can never imagine life without them. My childhood was filled with memories at our lake cabin in Wisconsin, vacations to places like Colorado, Canada, and Grand Cayman, and most importantly, partying like pirates on Halloween. To sum up my feelings in a few short words, my mom is more than my best friend and my dad is larger than life. I can’t forget my amazing sisters Carley and Kris, and my best brother Tim too. (I promise I’ll get to talking about how this relates to neuroscience, and ignore the shoutouts if you want, but being in a city thriving on emotion has me feeling very sentimental!)

In order to recognize the faces of people that you are familiar with, your brain has created special networks for processing this visual information (Arsalidou et al., 2010). This especially holds true for the faces of parents. On either side of the brain, people have two areas known as the fusiform gyri that are thought to help recognize faces (Barton et al., 2002). The fusiform gyrus on the right side of the brain has been noted to be especially important in recognizing facial configuration (Barton et al., 2002). When this part of the brain is damaged, people present symptoms of prosopagnosia and cannot recognize faces (Barton et al., 2002). Due to an underlying emotional connection children typically have with their parents, other areas of the brain beyond the fusiform gyrus have been implicated in recognizing the two familiar faces of their parents (Arsalidou et al., 2010).

The highlighted part shows the fusiform gyrus

One of the cruxes of the study of parental face recognition performed by Arsalidou and associates in 2010 hinged upon the subjects growing up living with both parents, having both parents alive at the time of the study, and remaining in regular contact with their parents (Arsalidou et al., 2010). For people who grew up raised by another important adult figures, these areas of the brain may or may not be activating in the same way, but that was not considered as a part of this study (Arsalidou et al., 2010). The areas of the brain that activated when looking at the faces were measured by functional magnetic resonance imaging (fMRI) (Arsalidou et al., 2010). fMRI is a non-invasive way to measure the change in blood flow to certain regions in the brain; areas with the most blood flow are considered to be the most activated during a specific task.

When looking at pictures of their mother, the subjects’ fMRI scans showed the most parts of the brain being activated compared to all other presented faces (Arsalidou et al., 2010). This extensive activation suggests that the mother’s face is the most important face a person can recognize (Arsalidou et al., 2010). Many structures including the middle temporal gyrus and inferior frontal gyrus were activated in comparison to known, but not personally relevant, celebrity female faces (Arsalidou et al., 2010). These areas of the brain are located near the fusiform gyrus within the temporal lobe, which is located on the side of the brain (Arsalidou et al., 2010). The activation of the middle temporal and inferior frontal gyrus when looking at your mother’s face, areas thought to be related to processing recognition of your own face, seems to show that there may be an overlap in processing both the face of your mother and the appearance of your own face (Arsalidou et al., 2010). This may be due to an overlap between memories of your mother with memories you have of yourself given the very strong emotional attachment between mother and child (Arsalidou et al., 2010).

The highlighted part shows the temporal lobe

The faces of fathers specifically activated the caudate when compared to other known, but not personally applicable, celebrity males (Arsalidou et al., 2010). The caudate is a brain area associated with the memory of feelings of love or reward (Arsalidou et al., 2010). This brain structure was also active when the subjects looked at their mothers’ faces; however, other brain structures were more predominantly active than the caudate (Arsalidou et al., 2010). The caudate appears to contribute to a feeling of endearment we have towards our parents (Arsalidou et al., 2010).

The highlighted structure is the caudate

To sum up the findings, distinct patterns of areas in your brain are activated when you see the faces of people you are attached to, like your mother and father. From an evolutionary standpoint, this is very important for recognizing the people who will love and take care of you from every single other person in the world (Arsalidou et al., 2010). Greater activation when looking at your mother’s face may be due to the extensive emotional memory connection between a mother and child (Arsalidou et al., 2010). Significant activation in the caudate from seeing your father’s face may indicate our feeling of paternal love (Arsalidou et al., 2010). These patterns of activation are very important to a human being given the highly social nature of our species and how much we are emotionally attached to the people who raise us.

So, for the two people who have loved me more than anyone else in the world, I happily left a lock on the bridge. While I can’t wait to return home and have my brain activated in the specific patterns that only looking at the faces of my mother and father can do, I have a new appreciation of the amount of love shown in various ways throughout this city. I plan on enjoying every aspect of my last two weeks here, and hope to stumble upon more treasures like this bridge. No one in my family has ventured to Europe before I took this trip, and I hope that I can someday bring them back to show them the lock I left on the bridge for all of us.

Lots and lots of locks

Lots and lots of locks

One in a million

Sending my love all the way back to the crazy, fun, and cortically irreplaceable family I have back in Minnesota,

~ Emily Aidan Berthiaume

Works Cited

Arsalidou, M., Barbeau, E. J., Bayless, S. J., Taylor, M. J. (2010) Brain responses differ to faces of mothers and fathers. Brain and Cognition 74:47-51.

Barton, J. J.S., Press, D. Z., Keenan, J. P., O’Connor, M. (2002) Lesions of the fusiform face area impair perception of facial configuration in prosopagnosia. Neurology 58:71-78.

The Pont de Arts bridge is located to the right of the word "Seine" on the river

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Musée du Chocolat

Posted on June 18, 2013 by | 4 comments

Before I even set foot in Paris, I had an agenda to tend to—buy every friend and family member enough chocolate to hold them over until their own trip to France. As (arguably) the biggest dark chocolate fan on the east coast, I have gone out of my way to make sure I try chocolate (in all forms) from all over Paris. I have run the gamut by trying chocolate bars from our favorite local grocery store (shout out to Mono Prix) to inhaling the chocolate pastries sold at Ladurée. Tending to my chocolate cravings in Paris turned out to be much easier than expected…

Chocolate Pastries at Ladurée (yum)

Needless to say, I was beyond excited when I saw that a trip to a chocolate museum was conveniently worked into our syllabus a day-off activity. Probably a bit too excited, the other students and I worked our way through the Parisian Metro and RER systems and arrived at “Choco-Story – Le musée gourmand du chocolat” earlier this week. Walking into the hands-on museum, we were hit with a wave of the sweet scent of chocolate, instantly putting everyone in a better mood. Part of our museum experience involved a chocolate workshop where we actually learned how to make bite-sized chocolates, and we luckily got to package the chocolates to bring back to our dorm.

Chocolate Museum: 28 Boulevard de Bonne Nouvelle, 75010 Paris

After our workshop where we somehow managed to make chocolate without destroying the museum kitchen, we waited for the pieces to cool in the fridge. As soon as our chocolate was cooled and ready to eat, I instantly ate maybe one too many pieces. Regardless, I was completely satisfied with my experience at the museum and our homemade treats. At this point, I’m sure you’re wondering why a chocolate field trip was worked into our neuroscience syllabus. Chocolate, aside from being central to Parisian culture, is responsible for producing pleasurable, hedonic effects and can therefore activate various brain areas (Rolls 2005). It has, for this reason not only been used as an incentive in various animal experiments, but its’ effects on changing activity in different brain areas have also been studied.

The neuroscience student in me wondered why some students were not as excited as I was about our chocolate museum expedition. Doesn’t everyone love chocolate? Why are there some people who don’t have chocolate cravings? Current neuroscience research is exploring the physiological implications behind cravings, emphasizing the brain systems that control our food intake. It turns out that people, like me, who crave chocolate actually show heightened physiological reactivity to images of chocolate. This means that there are measured changes in blood flow in different areas of the brain (such as the orbitofrontal cortex, the insula, ventral striatum and midbrain) in response to chocolate pictures (Small et al., 2001). What does this mean for choco-holics?

Spilling chocolate all over the kitchen floor....

A recent study tested the actual brain activity differences across individuals who craved chocolate and those who didn’t have these characteristic cravings (Asmaro et al., 2012). Researchers recruited undergraduates and asked them to fill out a chocolate-craving questionnaire, which was used to objectively measure “chocolate cravings”. After taking all of the data from these questionnaires, the researchers categorized the participants into one of two groups: chocolate cravers and non-cravers. The behavioral task of this study involved showing three types of images to both groups of participants. Both non-cravers and cravers were shown images falling under the following categories: chocolate, neutral and target. The chocolate stimuli category had pictures of dark or milk chocolate (yum), the neutral category had pictures of bland, uncooked foods (like pasta, for example) and the target stimuli category included random pictures of chairs (Asmaro et al., 2012).

There were two main sessions for this study: before eating chocolate and after eating a delicious piece of chocolate. In each of the two sessions, 220 images (100 chocolate, 100 neutral and 20 chairs) were presented in blocks. The participants (in both groups) were told to keep their eyes fixed on the screen as these images came up, and as soon as a target picture (a chair) appeared, participants had to press a key on a keyboard. After this task, the participants were asked to rate their craving for chocolate on a scale of 1 to 5. While this task was going on, researchers had an electroencephalogram along the patient’s scalp. An electroencephalogram is simply a tool that neuroscientists use to measure and record the electrical activity in the human brain. The reason they used an electroencephalogram in this case was to have a way to measure the brain response to these different, presented images. This actual brain response is commonly referred to as an “event-related potential” (Asmaro et al., 2012).

The researchers found that when the chocolate craving group was presented with a picture of chocolate, their brain activity indicated that they had a greater desire for chocolate overall. The non-craving group, however, had a lesser desire for chocolate after the task (Asmaro et al., 2012). This shows that presenting the chocolate stimuli actually caused different neurological responses across the two groups—cravers and non-cravers. If we take a step back and apply this back to my chocolate obsession, it is probable that I may have had different areas of my brain activated when I walked into the chocolate museum and saw all of the chocolate merchandise and pictures (when compared to some of my not so excited classmates).

Cooling chocolate (the French way...)

Asmaro et al. (2012) also showed that in non-cravers, the early changes in an area of the brain disappeared after eating some chocolate. This suggests that certain brain mechanisms control the otherwise natural urge to continue to eat chocolate in non-cravers (Asmaro et al., 2012). In cravers, however, a similar area of the brain (the orbitofrontal cortex) showed no changes in activity even after eating chocolate. What does this mean for us chocolate lovers, then? Turns out certain areas in our brain, such as the orbitofrontal cortex, are more likely to tell us to stop eating chocolate if we are classified as a “non-craver”. For us cravers, however, chocolate is a “wanted stimulus with a high motivational value” (a value that we subjectively place on it) and so our brains don’t really tell us to stop as readily as the brains of our fellow non-cravers. This is due to the fact that we have grown to appreciate and place immense value on chocolate.

Turns out, studies on the effects of chocolate on the brain are quite popular—mainly because they provide us with insight on consummatory and dietary patterns in humans.  The question is now: are you a craver or non-craver, and what are you going to do about it? If you’re anything like me, I’ll see you at the local bakery scoping out the best chocolate pastries.

 

-Noareen Ahmed

 

References:

Asmaro D, Fern J, Valery S, Isabel T, Patrick C, Mario L (2012) Spatiotemporal dynamics of the hedonic processing of chocolate imags in individuals with and without trait chocolate craving. Appetite 58: 790-799.

Rolls E, McCabe C (2007). Enhanced affective brain activations of chocolate in         cravers vs. non-cravers. European Journal of Neuroscience 26: 1067–1076

Small D, , Zatorre R, Dagher A, Evans A, Jones-Gotman M (2001). Changes in brain activity related to eating chocolate. From pleasure to aversion. Brain, 124: 1720–1733.

 

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Parisian Basketball: Where’s the ball?

Posted on June 12, 2013 by | 3 comments

I love basketball. Beyond the flashy dunks and glitzy ego-driven trash talk lies sophistication and balance. The harmonious and smooth movement of the ball around the player and around the court can be mesmerizing. However, while fancy dribbling and acrobatic athleticism may inundate the highlight reels, the true beauty of the game lies in the simple versatility of ball movement, or in other words, how you handle the basketball while on the court. How can we move the ball without making a mistake and giving the other team a chance to take it back? This question came to mind when I stepped on the court a few days ago. Since being in Paris, I knew I would miss the game too much to stop myself from playing: I had to play, even if I couldn’t speak the language. Lucky for me, I found a small park across the street from the Cite U. with a basketball court. Without saying a word, I pointed to the ball and then pointed to myself. The guys on the court nodded their heads in approval as I stepped up and played in a game.

Parisian Basketball Court

While I was a bit anxious to be playing in another country in a game that requires teamwork and communication, all the stress faded away as I caught a pass and put up an easy open shot close to the rim. While my teammates and I couldn’t really say much of anything to each other, we were in perfect unison. We knew what we were all doing as we were scrambling around the court, trying to deceive our opponents with subtle movements and sharp explosions for open positioning.

Good basketball isn’t precedent on what’s shown on the big screen. It’s about teamwork, and teamwork is manifested through good passing. Together as a team, we work as a cohesive unit to pass the ball before eventually shoot a high-percentage shot. What’s easier, an open shot 2 feet from the rim, or a behind the back, 360 spin shot 20 feet away? Passing is what is essential for success and playing with these guys, where grounded fundamentals overtake acrobatic athleticism, makes the game so much fun as an outsider.

So what do you need to do to make a good pass? In a game that has so many variables, it’s easy to get distracted. You have to consider so many things and not only understand the movement of your own players, but also the actions of your opponents to be able to synthesize that information and make an affirmative decision. This consideration and process is an example of working memory, or the ability to hold multiple pieces of information (i.e. position and movement of players) and then manipulate that information for further comprehension (i.e. the guy on my left will be open for a pass soon) (Furley, 2013). As much as want to retain the relevant information to make a good decision, we conversely want to exclude the unnecessary information. When playing basketball or any other goal-driven task, who cares what color someone’s eyes are or what that green stuff stuck in their teeth is. If our brains readily accepted every detail, our minds would be too overwhelmed with all that information. Therefore, we filter out what’s needed and what’s not. This process of focusing on the important stuff while paying little attention to the unimportant details that come from our senses is known as top-down modulation (Zanto, 2009). Furthermore, this modulation is greatly tied to attention and focus. Through brain scans and other neural imaging, the evidence shows that there is an overlap in activity in the brain between what we place our attention on and our working memory (Zanto, 2009). Essentially, what we choose to emphasize as important (perhaps unknowingly) in a task will be more readily recalled and available as known information.

He has him beat

What I’ve just said should make sense– if we focus on something, we are better able to hold that information and use it. So what about distractions? Do they affect our performance somehow? One study tested the effect of ignoring irrelevant information in working memory performance. In the study, subjects were shown multiple videos of moving colored dots and then tested their working memory by asking them if a sample video matched what they stored in their memory. The subjects were broken up into 3 groups: some were told to remember color (but ignore motion), others were told to remember motion (but ignore color), and some were told to remember both. By measuring the brain activity while performing these tasks, the researchers found that those that performed poorly (based on a score that factored accuracy and time to recall) showed more brain activity in areas that correlated with the characteristic they were supposed to ignore, while those that performed well showed less activity in regions of the brain they were told to ignore (Zanto, 2009). By showing more activity in regions of the brain that should not be lit up (because they are not pertinent to the task), people that performed poorly did not show significant top-down modulation (the ability to focus, but ignore extraneous information), and the researchers concluded that neural suppression (low activity) of irrelevant information correlated with greater working memory performance.

To tie this back to basketball, making a good pass takes a lot of concentration, but it also requires factoring out what doesn’t matter. I would say this ability to discern what does and does not matter comes from experience and practice. By knowing what cues indicate an opening and what works and does not, basketball players are able to discern what information is necessary and what isn’t to make the right pass. Playing with the Parisians in a universal game was so much fun because they knew what passes to make and how to run around the court so that the ball could seamlessly move around the court and into the hoop. By ignoring the irrelevant information, which becomes more obvious through experience, they were perhaps able to optimize their working memory by effectively processing the important information to make the right pass and get the easy basket. As someone that can’t speak a lick of French, it’s weird how my team understood exactly what I was doing when I would be running on the court, looking for a pass. It seems like my body language was saying all it needed to say to play the game. How cool is that?

~Sam Yang

References:

Furley P, Memmert D (2013). “Whom should I pass to?” the more options the more attentional guidance from working memory. PLoS ONE 8 (5):e62278.

Zanto TP, Gazzaley A (2009). Neural suppresion of irrelevant information underlies optimal working memory performance. The Journal of neuroscience: the official journal of the Society for Neuroscience 29 (10): 3059-3066.

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Sorbet, what have you done to me?

Posted on June 12, 2013 by | 5 comments

Who would have ever thought that the garden of Versailles harbored the frozen ambrosia of the Gods? Perhaps it was also the very spot where the Garden of Eden was cultured. Whoever brought this gift from heaven, in the form of a sorbet, must have had compassion comparable to Mother Teresa. In simpler words, the sorbet I bought for 2.50 Euros was absolutely delicious. With its pleasing bright red color and slightly tart but not too tart aroma made my day. I had to buy another one as soon as I finished because of how empty my life felt. How did this simple sorbet bring such strong sensation to my taste buds?

Well we know there are molecules in food that code for sweet taste. Imagine the molecule as a baseball and the protein receptor as a catcher’s glove. When these molecules hit specific protein receptors, they attach to a specific type of cell (type 2) on your taste buds and cause a series of reactions called a signaling cascade. The end result of this cascade is the creation of a signal, called action potential, which causes a release of specific molecules called neurotransmitters.In this case, ATP was the neurotransmitter that was released. ATP then attaches to protein receptors on another cell that is a part of the pathway to the brain where the information of sweet taste is passed along. That pathway is referred to as the afferent gustatory neural pathway. Finally, the information is sent to the gustatory cortex, a part of the brain that finally tells you that the pastries shown below are sweet.

So that’s how the brain processes the sweetness of these macaroons. But that doesn’t explain why it was so good. Sweetness is only one aspect of the desert. There is also the bright colors, the sweet smell, and other combinations of tastes that make up the macaroons that I ordered. It is proposed that certain aspects of the sorbet become integrated at different parts of the brain. In the anterior insula, things like taste, smell, and texture of the food are integrated (Small, 2012). This information is then sent to the lateral hypothalamus, where you process how much you like the food (Li et al., 2013). This information is also sent to the thalamus to be enriched with detail such as the temperature. It is truly amazing how the brain is able to receive all of this information, process it in different areas of the brain, and combine it to form our perception of the world.

Now here’s something interesting to think about. Do you think your sweet tooth is indicative of social behavior? A novel study was done showing social behavior of rats that have been bred for low sweet intake versus rats that have been bred for high sweet intake. Results show that rats bred for high sweet intake show a more dominant personality via “king of the milk” competitions (Eaton et al., 2012). Could loving your sweets mean that you’re a more dominant person or could it cause some sort of behavioral change (epigenetics?) that causes you to act more dominant?

When I was eating these , I felt alive. Perhaps those were just pleasure receptors in my brain activating. But perhaps throughout the years, the amount of sweets that I have consumed has caused not only a physical change in me, but also a behavioral one.

~James Eun

References:

Eaton JM, Dess NK, Chapman CD (2012) Sweet success, bitter defeat: a taste phenotype predicts social status in selectively bred rats. PloS one 7:e46606.

Li JX, Yoshida T, Monk KJ, Katz DB (2013) Lateral hypothalamus contains two types of palatability-related taste responses with distinct dynamics. The Journal of neuroscience : the official journal of the Society for Neuroscience 33:9462-9473.

Small DM (2012) Flavor is in the brain. Physiology & behavior 107:540-552.

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