Sight Unseen

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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.

Photo credit: Pete Georgiev on Flickr under Creative Commons license

Plastic and the Developing Brain

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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

Flipping the Baby Switch

img_2348-1Rewind to last night. It was bedtime. My infant daughter was screaming and struggling in my lap while I tried to rock her to sleep. She pulled and twisted the skin on my face. She sunk her tiny teeth into my shoulder and chest. Exasperated, I rose from the rocker and started pacing around the nursery. Her tense little body instantly relaxed. Within ten seconds she was quiet and still. Within two minutes she was asleep.

The scene was not unusual for our household. Even as a newborn, my daughter was easy to upset and hard to soothe. When nothing else worked and I was about to lose my mind I’d get up and walk with her. Often the results were nothing short of miraculous. Imagine going from 100 miles per hour to zero in a snap. For those who recall the child android Vicki on the ‘80s TV show Small Wonder, think of the times someone flipped the off-switch on her back. That’s what it’s like when I walk with my daughter. Our aimless walking flips a switch somewhere inside of her. But how does the switch work? And why does she have one in the first place? A study published in Current Biology last month helps to explain this curious facet of infant behavior.

The head scientist behind the study was Dr. Kumi Kuroda at the RIKEN Brain Science Institute in Japan. As she described in an interview with ScienceNOW, she became interested in the topic when she noticed that she could calm her own newborn son by carrying him. She later tested 12 other newborns with their mothers and found that they behaved like her son. Overall, the effect was rapid and dramatic. Some babies stopped crying as soon as their mothers began to walk with them. The rest cried less and were less shrill when they did cry. The babies also moved less and had lower heart rates while they were being carried.

To study the biological mechanisms behind this remarkable calming response, Dr. Kuroda and her colleagues turned to mice. They showed that mouse pups have a similar response when carried by their mothers. Mouse moms carry their pups by the scruff of their necks. When carried, mouse pups less than 20 days old stop wriggling. Their heart rate slows and they stop crying out. (Like most mouse vocalizations, baby mouse cries are ultrasonic). They also draw their legs in when carried, making their bodies more compact for toting around.

Kuroda and colleagues investigated several physiological aspects of the calming response in mice. Only a few of these experiments are probably relevant for infants, since human babies don’t assume a compact position like carried mouse pups do. One looked for the triggers that make carried pups stop squirming. The scientists anesthetized the neck skin of baby mice and found that these animals wriggled more than untreated mouse pups when carried. They got the same result when they overdosed pups with vitamin B6 before testing. (Vitamin B6 overdose causes animals and humans to lose the sense of their body position and movement.) The upshot? For a mouse pup to stop wriggling when carried it must 1) sense that it’s being lifted and 2) sense that something is pulling on its neck skin. Take either sense away and the calming response disappears. My daughter may draw on similar senses to trigger her miraculous stillness while carried. (Only if you replace neck pulling with the pressure of my arms around her, of course. I don’t carry her by her neck skin, I swear.)

The scientists also wondered why a baby’s heart rate drops when it’s picked up and carried. To test this in mice, they gave pups a drug that turns down the parasympathetic nervous system (the set of nerves that return the body to a calm state after arousal). Pups treated with the drug still stopped wriggling when lifted, but their heart rates didn’t drop as they do in untreated pups. So while the parasympathetic nervous system slows down the carried pup’s (and possibly infant’s) heartbeat, it can’t take credit for other features of the calming response.

Clearly this calming response is more complicated than it seems. Many of my daughter’s brain areas, neural pathways, and sensory mechanisms were working in concert to soothe her last night as I walked her in circles. But why does she have this complex reaction to carrying in the first place? Grateful parents might imagine that the calming response evolved to keep us from going crazy, but unless going crazy involves committing infanticide, this explanation doesn’t hold water. Evolution doesn’t care whether parents are happy or well rested or have time to watch Game of Thrones. It only cares whether our offspring survive.

Dr. Kuroda and her colleagues propose that the calming response helped parents escape dangerous situations while protecting their young. According to this logic, calmer carried babies meant faster escapes and higher rates of survival. Certainly if you were running from a wild beast or a member of a rival village, holding a struggling infant might slow you down. Of course holding any infant would slow you down and it’s not clear that sprinting with a struggling newborn is much harder than lugging one that’s asleep.  The paper’s authors present little evidence to support their proposal, particularly in the context of human evolution. They point to a minor result with their mice that doesn’t easily translate to human behavior. In effect, the jury’s still out.

There are other possible explanations for the calming response, ones that don’t involve predators outrunning parents. Shushing can calm crying babies too, probably because it simulates an aspect of their environment in the womb (in this case,  physiological noise). The same could be true of walking with infants. The mothers in the Kuroda study held their babies against their chest and abdomen, which is also how I hold my daughter when I walk to soothe her. The type of movement she feels in that position is probably similar to the rocking and jostling she felt as a fetus in utero whenever I walked. If so, the calming response might be a result of early learning and comfort by association – a nice thought when you consider the gory alternative.

Each year at the end of May we find ourselves as far as possible from Thanksgiving Day. It can be something of a thankfulness drought. This May I am thankful for women in science and maternity leaves, computer-generated dragons and ’80s sitcom androids. And like Vicki’s parents, I am profoundly thankful that my daughter came furnished with an off-switch. Whatever the reason why.

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Photo credit: Sabin Dang

Esposito G, Yoshida S, Ohnishi R, Tsuneoka Y, Rostagno Mdel C, Yokota S, Okabe S, Kamiya K, Hoshino M, Shimizu M, Venuti P, Kikusui T, Kato T, & Kuroda KO (2013). Infant Calming Responses during Maternal Carrying in Humans and Mice. Current biology : CB, 23 (9), 739-45 PMID: 23602481

Pb on the Brain

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I’ve got lead on my mind. Lead the element, not the verb; the toxic metal that used to grace every gas tank and paint can in this grand country of ours. For the most part we’ve stopped spewing lead into our environment, but the lead of prior generations doesn’t go away. It lingers on the walls and windows of older buildings, on floors as dust, and in the soil. These days it lingers in my thoughts as well.

I started worrying about lead when my daughter became a toddler and began putting everything in her mouth. I fretted more when I learned that lead is far more damaging to young children than was previously thought. Even a tiny amount of it can irreversibly harm a child’s developing brain, leading to lower IQs, attention problems and behavioral disorders. You may never even see the culprit; lead can sit around as microscopic dust, waiting to be inhaled or sucked off of an infant’s fingers.

Public health programs use blood lead levels (BLLs) to evaluate the amount of lead in a child’s system and decide whether to take preventative or medical action. In the 1960s, only BLLs above 60 μg/dL were considered toxic in children. That number has been creeping downward ever since. In 1985 the CDC’s stated blood lead level of concern became 25 μg/dL and in 1991 it went down to 10. But last year the CDC moved the cutoff down to 5 μg/dL and got rid of the term “level of concern.” That’s because scientists now believe that any amount of lead is toxic. In fact, it seems as if lead’s neurotoxic effects are most potent at BLLs below 5 μg/dL. In other words, a disproportionately large amount of the brain damage occurs at the lowest doses. Recent studies have shown subtle intellectual impairments in kids with BLLs as low as 2 μg/dL (which is roughly the mean BLL of American preschoolers today). All great reasons for parents to worry about even tiny exposures to lead, no?

Yes. Absolutely. Parents never want to handicap their children, even if only by an IQ point or two. But here’s what’s crazy: nearly every American in their fifties, forties, or late-thirties today would have clocked in well over the current CDC’s cutoff when they were little. The average BLL of American preschoolers in the late ‘70s was 15 μg/dL – and 88% had BLLs greater than 10 μg/dL.

These stats made me wonder if whole generations of Americans are cognitively and behaviorally impaired from lead poisoning as children. Have we been blaming our intellectually underwhelming workforce on a mismanaged education system, cultural complacency, or the rise of television and video games when we should have been blaming a toxic metal element?

I was sure I wasn’t the first person to wonder about the upshot of poisoning generations of Americans. And lo and behold, a quick Google search led me to this brilliant article on Mother Jones from January. The piece chronicles a rise in urban crime that began in the ‘60s and fell off precipitously in the early-to-mid ‘90s nationwide. The author, Kevin Drum, walks readers through very real evidence that lead fumes from leaded gasoline were a major cause of the rise in crime (and that increased regulation restricting lead in gasoline could be credited for the sudden drop off.)

The idea certainly sounds far-fetched: generations of city-dwellers were more prone to violence as adults because they breathed high levels of lead fumes when they were kids. It doesn’t seem possible. But when you put the pieces together it’s hard to imagine any other outcome. We know that children of the ‘50s, ‘60s, and ‘70s had BLLs high enough to cause irreversible IQ deficits and behavioral problems (of which aggression and impulse control are particularly common). Why is it so hard to imagine that more of these children behaved violently when they became adults?

In the end, this terrible human experiment in mass poisoning has left me pondering two particular questions. First, what does it mean for generations of children to be, in a sense, retroactively damaged by lead? At the time, our levels were considered harmless, but now we know better. Does knowing now, at this point, explain anything about recent history and current events? Does it explain the remarkable intransigence of certain politicians or the bellicosity of certain talk show hosts, athletes, or drivers with a road rage problem? Aside from the crime wave, what other sweeping societal trends might be credited to the poisoning of children past? How might history have played out differently if we had all been in our right minds?

Finally, I’ve been thinking a lot about the leads and asbestoses and thalidomides of today. Pesticides? Bisphenol A? Flame retardants? What is my daughter licking off of those toys of hers and how is it going to harm her twenty years down the line? This is not just a question for parents. Think crime waves. Think lost productivity and innovation. Today’s children grow up to be tomorrow’s adults. Someday when we are old and convalescing they’ll take the reigns of our society and drive it heaven-knows-where. That makes child health and safety an issue for us all. We may never even know how much we stand to lose.

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Photo credit: Zara Evens

Feeling Invisible Light

7401773382_19963f6a8b_cIn my last post, I wrote about whether we can imagine experiencing a sense that we don’t possess (such as a trout’s sense of magnetic fields). Since then a study has come out that adds a new twist to our little thought experiment. And for that we can thank six trailblazing rats in North Carolina.

Like us, rats see only a sliver of the full electromagnetic spectrum. They can perceive red light with wavelengths as long as about 650 nanometers, but radiation with longer wavelengths (known as infrared, or IR, radiation) is invisible to them. Or it was before a group of researchers at Duke began their experiment. They first trained the rats to indicate with a nose poke where they saw a visible light turned on. Then the researchers mounted an IR detector to each rat’s head and surgically implanted tiny electrodes into the part of its brain that processes tactile sensations from its whiskers.

After these sci-fi surgeries, each rat was trained to do the same light detection task again – only this time it had to detect infrared instead of visible light. Whenever the IR detectors on the animal’s head picked up IR radiation, the electrodes stimulated the tactile whisker-responsive area of its brain. So while the rat’s eyes could not detect the IR lights, a part of its brain was still receiving information about them.

Could they do the new task? Not very well at first. But within a month, these adult rats learned to do the IR detection task quite well. They even developed new strategies to accomplish their new task; as these videos show, they learned to sweep their heads back and forth to detect and localize the infrared sources.

Overall, this study shows us that the adult brain is capable of acquiring a new or expanded sense. But it doesn’t tell us how the rats experienced this new sense. Two details from the study suggest that the rats experienced IR radiation as a tactile sensation. First, the post-surgical rats scratched at their faces when first exposed to IR radiation, just as they might if they initially interpreted the IR-related brain activity as something brushing against their whiskers. Second, when the scientists studied the activity of the touch neurons receiving IR-linked stimulation after extensive IR training, they found that the majority responded to both touch and infrared light. At least to some degree, the senses of touch and of infrared vision were integrated within the individual neurons themselves.

In my last post, I found that I was only able to imagine magnetosensation by analogy to my sense of touch. Using some fancy technology, the scientists at Duke were able to turn this exercise in imagination into a reality. The rats were truly able to experience a new sense by piggybacking on an existing sense. The findings demonstrate the remarkable plasticity of the adult brain – a comforting thought as we all barrel toward our later years – but they also provide us with a glimpse of future possibilities. Someday we might be able to follow up on our thought experiment with an actual experiment. With a little brain surgery, we may someday be able to ‘see’ infrared or ultraviolet light. Or we might just hook ourselves up to a magnificent compass and have a taste (or feel or smell or sight or sound) of magnetosensation after all.

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Photo credit: Novartis AG

ResearchBlogging.org

Thomson EE, Carra R, & Nicolelis MA (2013). Perceiving invisible light through a somatosensory cortical prosthesis. Nature communications, 4 PMID: 23403583

Be the Trout

1448187231_be85e17541_bMost of the time I forget that my mother lacks a sense of smell. It’s only when I complain about something stinky or comment on a delicious smell that I remember she isn’t sharing the experience with me. As I’ve mentioned before, my mother has never had a sense of smell, or at least none that she can ever remember. As a child, I often wondered how she might imagine the sensation of smell. Would she do it by analogy to her other senses? Would she be able to do it at all?

I returned to these musings from a different perspective recently when I read a scientific paper about trout. Trout, along with other migratory species from salmon to sea turtles and certain types of birds, enjoy a sense that we lack: magnetosensation. These animals perceive magnetic fields (including that of the Earth) and can use this information to orient themselves and navigate. The study’s authors found magnetic cells inside the noses of trout, each with tiny iron-containing crystals attached to their cell membranes. Thus, when a trout changed direction relative to the Earth’s magnetic field, these miniature magnets would presumably tug on the cell’s membrane in a way that the cell could detect and signal to other parts of the trout’s nervous system. The evolution of these wonderful little biological compasses may have been necessary for migrating animals to evolve on our planet and happily roam, return, and repeat.

So today I put myself in my mother’s shoes (or nose) and tried to imagine a sense I didn’t have. What would it be like to feel magnetic fields? I tried to embrace the role and be the trout. I closed my eyes and imagined my little trout self swimming around within a magnetic field that changed as I moved. How would that feel for the trout? My imaginative efforts were rewarded with a strong percept – flashes of tingling across the surface of my skin that mirrored my changes in direction. In essence, I could only imagine magnetosensation by analogy to somatosensation, the sense of touch. And this is almost certainly not what magnetosensation feels like to a trout. Not only do they already have a sense of touch akin to our own, but they also detect magnetic fields with their snout rather than their whole body.

It makes sense that I imagined a foreign sensation by analogy to one I know. Each of our senses has dedicated processing areas in the brain. Without a brain area developed for magnetosensation, it may not be possible to do any better than imagine it by way of the senses our brain can process. Or maybe it’s possible for people with more imaginative imaginations than my own. If you give it a try, please let me know what you come up with! And the next time you find yourself staring down a trout, tilapia, tuna, or salmon on your plate, spare a moment to appreciate that it has experienced a realm of sensations beyond your imagination. And then – bon appétit!

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Photo credit: sharkbait

ResearchBlogging.org

Eder SHK, Cadiou H, Muhamad A, McNaughton PA, Kirschvink JL, & Winklhofer M (2012). Magnetic characterization of isolated candidate vertebrate magnetoreceptor cells PNAS DOI: 10.1073/pnas.1205653109

At the Gates of Sleep

497736998_45c09a136e_oNow that my daughter is about to reach her first birthday, I’m in the mood to reflect on the year that just passed. Unfortunately, my recollections of it are a little fuzzy, probably because I can count on one hand the number of times I’ve enjoyed a good night’s sleep over the past year. Some people have babies who regularly sleep through the night and I am happy for them. Truly, I am. But clearly I was not meant to be in their ranks.

Still, the never-ending parade of nighttime awakenings has taught me something about my own brain. It is precisely tuned to hear my baby. Although I sleep blithely through my husband’s thunderous snoring and the loud buzz of his alarm clock – multiple times a day, thanks to the snooze button – I awaken at the faintest sound of my daughter’s sighs, coos, or grumbles. When she cries, I am immediately awake while my husband sleeps on beside me, undisturbed.

People are generally able to sleep through minor sounds and sensations thanks to a subcortical structure in the brain called the thalamus. This structure receives incoming signals from our senses and relays them to cortical areas devoted to processing sensory information like sounds or tactile sensations. When we’re awake, the thalamus faithfully relays nearly every sensory signal on to the cortex. But when we’re asleep, neurons in the thalamus participate in strong, synchronized waves of activity that squelch incoming signals. As a result, about 70% of these signals never make it to the cortex. This process, known as sensory-gating, is how we manage to sleep through the roar of rainstorms or the brush of the sheets against our skin each time we turn in bed. It is also how we sleep through our husband’s room-rattling snores.

Yet some sensory information does get through to the rest of the brain during sleep. These signals do get processed and can even wake us up if they are either intense (like a loud noise) or personally relevant. A clever study illustrated the importance of personal relevance by exposing sleeping subjects to a loud presentation (via tape recorder) of their own name spoken aloud. The scientists played the recording either normally or backwards and found that subjects awoke in less than half the time when they heard their names presented in the recognizable form.

So did my daughter, in effect, sleep train me by training my brain to recognize her sounds as personally relevant? It’s a plausible explanation, but one that is ultimately lacking. It cannot explain that first night when I slept beside my baby at the hospital nearly one year ago. Although I had labored through the entire night before and had not slept in the ensuing day, I awoke constantly to every little sound my mewing newborn made, not to mention the cries that told me she wanted to nurse. She’d had no time to train me; I had come pre-trained. Just as my breasts were primed to make milk for her, my brain was primed to wake for her. We seemed to be engineered for one other, mother and child, body and brain. And we spent that first long night discovering how clever a designer Nature can be, while my husband slept peacefully on the couch.

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Photo credit: planetchopstick

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