Tag Archives: neuroscience

Modernity, Madness, and the History of Neuroscience

September 7, 2013 By in Brains, Mental Illness, Minds, Science Tags: , , , , 12 Comments

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I recently read a wonderful piece in Aeon Magazine about how technology shapes psychotic delusions. As the author, Mike Jay, explains:

Persecutory delusions, for example, can be found throughout history and across cultures; but within this category a desert nomad is more likely to believe that he is being buried alive in sand by a djinn, and an urban American that he has been implanted with a microchip and is being monitored by the CIA.

While delusional people of the past may have fretted over spirits, witches, demons and ghouls, today they often worry about wireless signals controlling their minds or hidden cameras recording their lives for a reality TV show. Indeed, reality TV is ubiquitous in our culture and experiments in remote mind-control (albeit on a limited scale) have been popping up recently in the news. As psychiatrist Joel Gold of NYU and philosopher Ian Gold of McGill University wrote in 2012: “For an illness that is often characterized as a break with reality, psychosis keeps remarkably up to date.”

Whatever the time or the place, new technologies are pervasive and salient. They are on the tips of our tongues and, eventually, at the tips of our fingers. Psychotic or not, we are all captivated by technological advances. They provide us with new analogies and new ways of explaining the all-but-unexplainable. And where else do we attempt to explain the mysteries of the world, if not through science?

As I read Jay’s piece on psychosis, it struck me that science has historically had the same habit of co-opting modern technologies for explanatory purposes. In the case of neuroscience, scientists and physicians across cultures and ages have invoked the  innovations of their day to explain the mind’s mysteries. For instance, the science of antiquity was rooted in the physical properties of matter and the mechanical interactions between them. Around 7th century BC, empires began constructing great aqueducts to bring water to their growing cities. The great engineering challenge of the day was to control and guide the flow of water across great distances. It was in this scientific milieu that the ancient Greeks devised a model for the workings of the mind. They believed that a person’s thoughts, feelings, intellect and soul were physical stuff: specifically, an invisible, weightless fluid called psychic pneuma. Around 200 AD, a physician and scientist of the Roman Empire (known for its masterful aqueducts) would revise and clarify the theory. The physician, Galen, believed that pneuma fills the brain cavities called ventricles and circulates through white matter pathways in the brain and nerves in the body just as water flows through a tube. As psychic pneuma traveled throughout the body, it carried sensation and movement to the extremities. Although the idea may sound farfetched to us today, this model of the brain persisted for more than a millennium and influenced Renaissance thinkers including Descartes.

By the 18th century, however, the science world was a-buzz with two strange new forces: electricity and magnetism. At the same time, physicians and anatomists began to think of the brain itself as the stuff that gives rise to thought and feeling, rather than a maze of vats and tunnels that move fluid around. In the 179os, Luigi Galvani’s experiments zapping frog legs showed that nerves communicate with muscles using electricity. So in the 19th century, just as inventors were harnessing electricity to run motors and light up the darkness, scientists reconceived the brain as an organ of electricity. It was a wise innovation and one supported by experiments, but also driven by the technical advances of the day.

Science was revolutionized once again with the advent of modern computers in the 1940s and ‘50s. In the 1950s, the new technology sparked a surge of research and theories that used the computer as an analogy for the brain. Psychologists began to treat mental events like computer processes, which can be broken up and analyzed as a set of discrete steps. They equated brain areas to processors and neural activity in these areas to the computations carried out by computers. Just as computers rule our modern technological world, this way of thinking about the brain still profoundly influences how neuroscience and psychology research is carried out and interpreted. Today, some labs cut out the middleman (the brain) entirely. Results from computer models of the brain are regularly published in neuroscience journals, sometimes without any data from an actual physical brain.

I’m sure there are other examples from the history of neuroscience in general and certainly from the history of science as a whole. Please comment and share any other ways that technology has shaped the models, themes, and analogies of science!

Additional sources:

Crivellato E & Ribatti D (2007) Soul, mind, brain: Greek philosophy and the birth of neuroscience. Brain Research Bulletin 71:327-336.

Karenberg A (2009) Cerebral Localization in the Eighteenth Century – An Overview. Journal of the History of the Neurosciences, 18:248-253.

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Photo Credit: dominiqueb on Flickr, available through Creative Commons

Near-Death Experiment

August 15, 2013 By in Brains, Science Tags: , , , 3 Comments

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If you own a tv, radio, or computer, you’ve probably heard about the recent neuroscience experiment that studied after-death brain activity in rats. Perhaps you’ve seen it under titles like: Near-death experiences are ‘electrical surge in dying brain’ or Near-death experiences exposed: Surge of brain activity after the heart stops may trigger paranormal visions. You may have heard some jargon about brainwaves and frequency coupling or some such. What does it mean? It is time to chuck your rosary, or at least your copy of Proof of Heaven? (The answer to the latter, in case you’re wondering, is yes.)

The article that caused such a stir was penned by researchers at the University of Michigan and published in the scientific journal PNAS. The experiment was simple and so obvious that I immediately wondered why no one had done it before. The scientists implanted six electrodes in the surface of the rat’s brain. They recorded from the electrodes while the rat was awake and then anesthetized. Finally, they injected a solution into the rat’s heart to make it stop beating and recorded in activity in the rat’s brain while it died. None of these steps are unique. Neuroscientists often place electrodes in the brains of living rats and certainly lab rats are anesthetized and sacrificed on a daily basis. The crucial change that these scientists made was recording after the animal’s death.

What happened once its heart stopped?  A lot, probably more than anyone would have expected. In the first 30 seconds, the researchers observed rapid and coordinated neural activity in the rat’s brain. Unlike under anesthesia, when the rat’s brain was quieter than its wakeful norm, the dying brain was as active and, by some measures, more active than it was when fully awake and alive. We’re not talking about zombie rats here – this activity faded and disappeared beyond the 30-second window after cardiac arrest. Still, something dramatic and consistent happened in those dying moments. The brain activity was essentially the same across all nine rats that died from cardiac arrest and eight other rats that the scientists sacrificed using carbon dioxide inhalation. The results were no fluke.

Of course, these findings (and the headlines touting them in the news) beg the question: is this activity the neural basis for near-death experiences? The answer, of course, is we don’t know. We obviously can’t ask the rats what they experienced, if they experienced anything at all. Still, the activity during the 30-second window wasn’t drastically different from the brain’s wakeful activity, at least according to some of their measures. It’s certainly possible, maybe even probable, that the rat experienced something during this time. That fact alone is intriguing. To say more, we’ll need more grants, more studies, and more dead rats.

For the time being, I’m sure people will spin these results according to their pre-existing beliefs. Some will probably say that the brain activity at death is the physiological echo of God coaxing the soul from the body. And who am I say it ain’t so? But there are certainly other explanations. Neural rhythms arise naturally from the wiring of the brain. Neurons form an incredible number of circuits, or wiring loops, that reverberate. Each neuron is a complex little creature in its own right: electrically charged, tiny, tentacled, and bustling with messenger molecules, neurotransmitters, and ions. When neurons are deprived of oxygen and energy, their electrical charges change drastically, which can cause them to fire errant signals at each other. Without input from the outside world, these errant signals may harmonize in ways that reflect the internal wiring of the system. It’s a little like playing a trumpet. When you blow into the trumpet, your breath is a chaotic rush of air, yet it emerges as a clear and orderly tone. An organized system can make order out of chaos. The same might be said of your brain. And if it turns out that this type of coordinated brain activity actually does cause a special experience when you die, consider it an accidental symphony that plays you one last song before you go.

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Photo credit: Paul Stocker on Flickr, used via Creative Commons license

ResearchBlogging.org

Borjigin J, Lee U, Liu T, Pal D, Huff S, Klarr D, Sloboda J, Hernandez J, Wang MM, & Mashour GA (2013). Surge of neurophysiological coherence and connectivity in the dying brain. Proceedings of the National Academy of Sciences of the United States of America PMID: 23940340

Eyes Wide Shut

August 3, 2013 By in Brains, Science Tags: , , 8 Comments

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In the middle of the 20th century, experimental psychologists began to notice a strange interaction between human vision and time. If they showed people flashes of light close together in time, subjects experienced the flashes as if they all occurred simultaneously. When they asked people to detect faint images, the speed of their subjects’ responses waxed and waned according to a mysterious but predictable rhythm. Taken together, the results pointed to one conclusion: that human vision operates within a particular time window – about 100 milliseconds, or one-tenth of a second.

This discovery sparked a controversy about the nature of vision. Pretty much anyone with a pair of eyes will tell you that vision feels smooth and unbroken. But is it truly as continuous as it feels, or might it occur in discrete chunks of time? Could the cohesive experience of vision be nothing more than an illusion?

Enthusiasm for the idea of discrete visual processing faded over the years, although it was never disproven. Science is not immune to fads; ideas often fall in and out of favor. Besides, vision-in-chunks was a hard sell. It was counterintuitive and contrary to people’s subjective experience. Vision scientists set it aside and moved on to new questions and controversies instead.

The debate resurfaced in the last twenty years, sparked by the discovery of a new twist on an old optical illusion. Scientists have long known about the wagon wheel illusion, which makes it appear as if the wheels of moving cars (or wagons) in films are either turning in the wrong direction or not turning at all. The illusion is caused by a technical glitch: the combination of the periodic rotating wheel and the frame rate of the movie. Your brain doesn’t get enough examples of the spinning wheel to know its direction and speed. But in 1996, scientists discovered that the illusion also occurred in the real world. When hubcaps, tires, and modified LPs turned at certain rates, their direction appeared to reverse. Scientists dug the idea of discrete vision out of a trunk in the attic, dusted it off, and tried it out to explain the effect. In essence, the visual system might have a frame rate of its own. Cross this frame rate with an object rotating at a certain frequency and you’re left seeing tires spin backwards. It seemed to make sense.

In a clever set of experiments, the neuroscientist and author David Eagleman (of Incognito and Sum fame) shot this explanation down. He and his colleague, Keith Kline, chalked the illusion up to tiring motion-processing cells instead. Still, the debate about the nature of vision was reignited. Several neuroscientists became intrigued with the notion of vision-in-chunks and began to think about it in relation to a particular type of brain rhythm that cycles at a rate of – you guessed it – about ten times per second.

In recent years, a slew of experiments have supported the idea that certain aspects of vision happen in discrete packets of time – and that these packets are roughly one-tenth of a second long. The brain rhythms that correspond to this timing – called alpha waves – have acted as the missing link. Brain rhythms essentially tamp down activity in a brain area at a regular interval, like a librarian who keeps shushing a crowd of noisy kids. Cells in a given part of the brain momentarily fall silent but, as kids will do, they start right up again once the shushing is done.

Work by Rufin VanRullen at the Université de Toulouse and, separately, by Kyle Mathewson at the University of Illinois show how this periodic shushing can affect visual perception. For example, Mathewson and colleagues were able to predict whether a subject would detect a briefly flashed circle based on its timing relative to the alpha wave in that subject’s visual cortex. This and other studies like it demonstrate that alpha waves are not always helpful. If something appears at the wrong moment in your rhythm, you could be slower to see it or you might just miss it altogether. In other words, every tenth of a second you might be just a little bit blind.

If you’re a healthy skeptic, you may be wondering how well such experiments reflect vision in the real world. Unless your computer’s on the fritz, you probably don’t spend much time staring at circles on a screen. Does the 10-per-second frame rate apply when you’re looking at the complex objects and people that populate your everyday world?

Enter Frédéric Gosselin and colleagues from the Université de Montréal. Last month they published a simple study in the journal Cognition that tested the idea of discrete vision using pictures of human faces. They made the faces hard to see by bathing them in different amounts of visual ‘noise’ (like the static on a misbehaving television). Subjects had to identify each face as one of six that they had learned in advance. But while they were trying to identify each face, the amount of static on the face kept changing. In fact, Gosselin and colleagues were cycling the amount of static to see how its rate and phase (timing relative to the appearance of each new face) affected their subjects’ performance. They figured that if visual processing is discrete and varies with time, then subjects should perform best when their moments of best vision coincided with the moments of least static obscuring the face.

What did they find? People were best at identifying the faces when the static cycled at 10 or 15 times per second. Gosselin and colleagues suggest that the ideal rate may be somewhere between the two (a possibility that they can’t test after-the-fact). Their results imply that the visual alpha wave affects face recognition – a task that people do every day. But it may only affect it a little. The difference between the subjects’ best accuracy (when the static cycling was set just right) and their worst accuracy was only 7%. In the end, the alpha wave is one of many factors that determine perception. And even when these rhythms are shushing visual cortex, it’s not enough to shut down the entire area. Some troublemakers keep yapping right through it.

When it comes to alpha waves and the nature of discrete visual processing, scientists have their work cut out for them. For example, while some studies found that perception was affected by an ongoing visual alpha wave, others found that visual events (like the appearance of a new image) triggered new alpha waves in visual cortex. In fact, brain rhythms are not by any means exclusive; different rhythms can be layered one upon the other within a brain area, making it harder to pull out the role of any one of them.  For now it’s at least safe to say that visual processing is nowhere near as smooth and continuous as it appears. Your vision flickers and occasionally fails. As if your brain dims the lights, you have moments when you see less and miss more – moments that may happen tens of thousands of times each hour.

This fact raises a troubling question. Why would the brain have rhythms that interfere with perception? Paradoxically enough, discrete visual processing and alpha waves may actually give your visual perception its smooth, cohesive feel. In the last post I mentioned how you move your eyes about 2 or 3 times per second. Your visual system must somehow stitch together the information from these separate glimpses that are offset from each other both in time and space. Alpha waves allow visual information to echo in the brain. They may stabilize visual representations over time, allowing them to linger long enough for the brain, that master seamstress, to do her work.

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Photo credit: Tom Conger on Flickr with Creative Commons license

Blais C, Arguin M, & Gosselin F (2013). Human visual processing oscillates: Evidence from a classification image technique Cognition, 128 (3), 353-62 PMID: 23764998

Sight Unseen

August 1, 2013 By in Brains, Science Tags: , , , 1 Comment

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Eyelids. They come in handy for sandstorms, eye shadow, and poolside naps. You don’t see much when they’re closed, but when they’re open you have an all-access pass to the visible world around you. Right? Well, not exactly. Here at Garden of the Mind, the next two posts are dedicated to the ways that you are blind – every day – and with your eyes wide open.

One of the ways you experience everyday blindness has to do with the movements of your eyes. If you stuck a camera in your retina and recorded the images that fall on your eye, the footage would be nauseating. Think The Blair Witch Project, only worse. That’s because you move your eyes about once every half a second – more often than your heart beats. You make these eye movements constantly, without intention or even awareness. Why? Because, thanks to inequalities in the eye and visual areas of the brain, your peripheral vision is abysmal. It’s true even if you have 20/20 vision. You don’t sense that you are legally blind in your peripheral vision because you compensate by moving your eyes from place to place. Like snapping a series of overlapping photographs to create a panoramic picture, you move your eyes to catch different parts of a scene and your brain stitches these ‘shots’ together.

As it turns out, the brain is a wonderful seamstress. All this glancing and stitching leaves us with a visual experience that feels cohesive and smooth – nothing like the Frankenstein creation it actually is. One reason this beautiful self-deception works is that we turn off much of our visual system every time we move our eyes. You can test this out by facing a mirror and moving your eyes quickly back and forth (as if you are looking at your right and left ears). Try as you might, you won’t be able to catch your eyes moving. It’s not because they’re moving too little for you to see; a friend looking over your shoulder would clearly see them darting back and forth. You can feel them moving yourself if you gently rest your fingers below your lower lashes.

It would be an overstatement to say that you are completely blind every time you move your eyes. While some aspects of visual processing (like that of motion) are switched off, others (like that of image contrast) seem to stay on. Still, this means that twice per second, or 7,200 times each hour, your brain shuts you out of your own sense of sight.  In these moments you are denied access to full visual awareness. You are left, so to speak, in the dark.

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Photo credit: Pete Georgiev on Flickr under Creative Commons license

Plastic and the Developing Brain

July 12, 2013 By in Brains, Pregnancy Tags: , , , , 1 Comment

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When I was pregnant with my daughter, I had enough on my mind. I didn’t have much time to think much about plastic. I knew vaguely that plastics can release estrogen-mimicking substances like bisphenol A (BPA) into our food and I’d heard that they might cause genital defects in male fetuses. But once my husband and I had the 20-week ultrasound and knew we were having a girl, I thought I could stop searching for products in cardboard or glass. It was just too hard. Everything is packaged in plastic these days.

Apparently I jumped the gun.

Scientific papers warning about the hazards of prenatal exposure to BPA have been coming out in a steady stream, with a string of particularly damning ones appearing over the last 18 months in the Proceedings of the National Academy of Sciences. Last month one in particular caught my eye: a study of how prenatal BPA exposure changes the brain. The results were enough to make this neuroscientist pause.

While we tend to think of estrogens as the sex hormones that manage ovulation and pregnancy, these molecules also have powerful and direct effects on the brain. Many types of neurons have estrogen receptors on their outer surface. While there are several kinds of estrogen receptors in the brain, all bind to estrogens (and other molecules that resemble estrogens) and all trigger changes within their neurons as a result. These small changes can potentially add up to alter how entire neural circuits function. In fact, estrogens influence a wide range of skills and behaviors – from cognitive function to mood regulation and even fine motor control. While we don’t yet know why estrogens have such a broad and powerful influence on the brain, it does appear that we should think twice before mucking around with estrogen levels, particularly in the developing brain.

BPA and other compounds found in plastics resemble estrogens. The similarity is close enough to fool estrogen receptors, which bind to these foreign molecules and interpret them as additional estrogen. Although BPA has been used commercially as a dental sealant and liner for food containers (among many other uses) since the 1960s, the health consequences of this case of mistaken identity are just beginning to be understood.

In the PNAS paper published last month, a group of scientists headed by Dr. Frances Champagne at Columbia report the effect of prenatal BPA exposure on mice. They fed pregnant laboratory mice one of three daily doses of BPA (2, 20, or 200 μg/kg) or a control product without BPA. These are not high doses of BPA. Based on the amount of BPA found in humans, scientists estimate that we are exposed to about 400 μg/kg per day. The U.S. Food and Drug Administration reached their own estimate by testing the amount of BPA in various foods and then approximating how much of these people consume daily. Their calculations put the figure at around 0.19 μg/kg daily for adults. This discrepancy (400 versus 0.19) is one of many points of contention between the FDA, the packaging industry, and the scientific community on the subject of BPA.

Champagne and her colleagues fed their mice BPA on each of the twenty days of mouse gestation. (That’s right, ladies: mouse pregnancies last less than three weeks.) After each mouse pup was born, the scientists either studied its behavior or sacrificed it and examined its brain.

What did they find? Prenatal BPA exposure had a noticeable impact on mouse brains, even at the lowest dose. They found BPA-induced changes in the number of new estrogen receptors being made in all three brain areas they examined: the prefrontal cortex, hypothalamus, and hippocampus. These effects were complex and differed depending on the gender of the animal, the brain area, the BPA dose, and the type of estrogen receptor. Still, in several cases the researchers found a surprising pattern. Without BPA-exposure, female mice typically made more new estrogen receptors than their male counterparts. The same was true for mice given the highest BPA dose. But among pups exposed to the two lowest BPA doses, male mice made more estrogen receptors than females! This sex-difference reversal stemmed from changes in both genders; male mice made more estrogen receptors than normal at these doses while female mice made fewer than their norm.

Champagne and colleagues also observed and recorded several behaviors of the mice in different circumstances. For most behaviors, males and females were naturally different from one another.  Just as human boys tend to chase each other more than girls do, male mouse pups chased more than females. Unexposed male mice sniffed a new mouse more than unexposed females did. They showed more anxiety-like behavior in an open space and were less active in their home cages. Prenatal BPA treatment reversed these natural sex differences. Exposed female mice did more sniffing, acted more anxious, and ran around less than their exposed male counterparts. And at the highest prenatal BPA dose, the male mice chased each other as rarely as the females did. In one case, BPA treatment affected the two genders similarly; both sexes were less aggressive than normal at the two lower doses and more aggressive than normal at the highest dose.

Overall, the results of the study are complex and it might be easy to ignore them because they don’t seem to tell a straightforward tale. Yet their findings can be summed up in a single sentence: BPA exposure in utero has diverse effects on the mouse brain and later behavior. Not only does the BPA ingested by the mom manage to affect the growing fetus, but those effects persist beyond the womb and past the end of the exposure to BPA.

Some will dismiss these results because they come from mice. After all, how much do we really resemble mice? Yet studies in monkeys have also found that BPA affects fetal development. And while mice and monkeys excrete BPA differently, they clear it at a similar rate — to each other and to human women. Results from correlational studies in humans also suggest that BPA exposure during development affects mood, anxiety and aggressiveness to varying degrees (depending on the child’s gender).

Still, there’s a lot we don’t know about the relevance of this study for humans. At the end of the day, mice aren’t humans and no one has agreed on how much BPA pregnant women ingest. Moreover, Champagne and colleagues examined only a small subset of the neural markers and behaviors that BPA might affect in mice. Perhaps the changes they describe are the worst of BPA’s effects, or perhaps they are only the tip of the iceberg. We don’t yet know.

What’s the upshot of all this? You may want to err on the side of caution, particularly if you’re pregnant. Avoid plastics when possible. Be aware of other sources of BPA like canned foods (which have plastic liners) and thermal receipts. Do what you can do and then try not to let it stress you out. If you’re pregnant, you already have enough on your mind.

As for my daughter, she seems to be fine despite her plasticized third trimester. While she doesn’t do much sniffing, she does occasionally slap my husband or me in the face. It could be the BPA making her aggressive. I choose to blame it on her sassy genes instead.

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Photo credit: .imelda on Flickr

ResearchBlogging.org

Kundakovic M, Gudsnuk K, Franks B, Madrid J, Miller RL, Perera FP, & Champagne FA (2013). Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure. Proceedings of the National Academy of Sciences of the United States of America, 110 (24), 9956-61 PMID: 23716699