The Top 5 Neuroscience Breakthroughs of 2012

More than any year before, 2012 was the year neuroscience exploded into pop culture. From mind-controlled robot hands to cyborg animals to TV specials to triumphant books, brain breakthroughs were tearing up the airwaves and the internets. From all the thrilling neurological adventures we covered over the past year, we’ve collected five stories we want to make absolutely sure you didn’t miss.

Now, no matter how scientific our topic is, any Top 5 list is going to turn out somewhat subjective. For one thing, we certainly didn’t cover every neuroscience paper published in 2012 – we like to pick and choose the stories that seem most interesting to us, and leave the whole “100 percent daily coverage” free-for-all to excellent sites like ScienceDaily.

As you may’ve also noticed, we tend to steer clear of headlines like “Brain Region Responsible for [X] Discovered!” because – as Ben talks about with Matt Wall in this interview – those kinds of discoveries are usually as vague and misleading as they are overblown by the press.

Instead, we chose to focus on five discoveries carry some of the most profound implications of any research published this past year – both for brain science, and for our struggle to understand our own consciousness.

So on that note, here – in countdown order – are the five discoveries that got us the most pumped up in 2012!


5. A Roadmap of Brain WiringA grid of fibers, bein' all interwoven and stuff.

Neuroscientists like to compare the task of unraveling the brain’s connections to the frustration of untangling the cords beneath your computer desk – except that in the brain, there are hundreds of millions of cords, and at least one hundred trillion plugs. Even with our most advanced computers, some researchers were despairing of ever seeing a complete connectivity map of the human brain in our lifetimes. But thanks to a team led by Van Wedeen at the Martinos Center for Biomedical Imaging at Massachusetts General Hospital, 2012 gave us an unexpectedly clear glimpse of our brains’ large-scale wiring patterns. As it turns out, the overall pattern isn’t so much a tangle as a fabric – an intricate, multi-layered grid of cross-hatched neural highways. What’s more, it looks like our brains share this grid pattern with many other species. We’re still a long way from decoding how most of this wiring functions, but this is a big step in the right direction.


Opto Brain Blue_49704. Laser-Controlled Desire

Scientists have been stimulating rats’ pleasure centers since the 1950s – but 2012 saw the widespread adoption of a new brain-stimulation method that makes all those wires and incisions look positively crude. Researchers in the blossoming field of optogenetics develop delicate devices that control the firing of targeted groups of neurons – using only light itself. By hooking rats up to a tiny fiber-optic cable and firing lasers directly into their brains, a team led by Garret D. Stuber at the University of North Carolina at Chapel Hill School of Medicine were able to isolate specific neurochemical shifts that cause rats to feel pleasure or anxiety – and switch between them at will. This method isn’t only more precise than electrical stimulation – it’s also much less damaging to the animals.

(Thanks again, Mike Robinson, for sharing this image of your team’s laser-controlled brain!)


3. Programmable Brain Cells

7d1-chk-nf-h-3Pluripotent stem cell research took off like a rocket in 2012. After discovering that skin cells can be genetically reprogrammed into stem cells, which can in turn be reprogrammed into just about any cell in the human body, a team led by Sheng Ding at UCSF managed to engineer a working network of newborn neurons from a harvest of old skin cells. In other words, the team didn’t just convert skin cells into stem cells, then into neurons – they actually kept the batch of neurons alive and functional long enough to self-organize into a primitive neural network. In the near future, it’s likely that we’ll be treating many kinds of brain injuries by growing brand-new neurons from other kinds of cells in a patient’s own body. This is already close on the horizon for liver and heart cells – but the thought of being able to technologically shape the re-growth of a damaged brain is even more exciting.


microchip2. Memories on Disc

We’ve talked a lot about how easily our brains can modify and rewrite our long-term memories of facts and scenarios. In 2012, though, researchers went Full Mad Scientist with the implications of this knowledge, and blew some mouse minds in the process. One team, led by Mark Mayford of the Scripps Research Institute, took advantage of some recently invented technology that enables scientists to record and store a mouse’s memory of a familiar place on a microchip. Mayford’s team figured out how to turn specific mouse memories on and off with the flick of a switch – but they were just getting warmed up. The researchers then proceeded to record a memory in one mouse’s brain, transfer it into another mouse’s nervous system, and activate it in conjunction with one of the second mouse’s own memories. The result was a bizarre “hybrid memory” – familiarity with a place the mouse had never visited. Well, not in the flesh, anyway.


1. Videos of Thoughts

reconstruct1Our most exciting neuroscience discovery of 2012 is also one of the most controversial. A team of researchers from the Gallant lab at UC Berkeley discovered a way to reconstruct videos of entire scenes from neural activity in a person’s visual cortex. Those on the cautionary side emphasize that activity in the visual cortex is fairly easy to decode (relatively speaking, of course) and that we’re still a long, long way from decoding videos of imaginary voyages or emotional palettes. In fact, from one perspective, this isn’t much different from converting one file format into another. On the other hand, though, these videos offer the first hints of the technological reality our children may inhabit: A world where the boundaries between the objective external world and our individual subjective experiences are gradually blurred and broken down. When it comes to transforming our relationship with our own consciousness – and those of the people around us – it doesn’t get much more profound than that.


So there you have it: Our picks for 2012’s most potentially transformative neuroscience breakthroughs. Did we miss an important one? Did we overstate the importance of something? Almost certainly, yes. So jump into the comments and let us know!


Deciphering Sleep: Our Interview with David Rye

Why do we need to sleep? In all of human biology, few questions are more persistent – or more mythologized – than this one. Almost as puzzling as sleep itself are sleep disorders like narcolepsy and insomnia, which make us wonder why some of us need so much more sleep than others do.

David Rye, a neurologist at Emory University’s School of Medicine, thinks he may finally have some answers to these age-old questions. While studying hypersomnia, an unusual disorder characterized by long yet unsatisfying sleep, David and his co-researchers discovered a new brain chemical that may not only be responsible for hypersomnia, but could help explain why we need to sleep at all.

As soon as I read David’s paper, I knew I had to call him up and talk in more detail. I think you’ll agree that his ideas could turn out to have big implications for all of us.    –Ben
Ben Thomas: How’d you get interested in studying hypersomnia, David? Was there a particular patient…?

David Rye: Any sleep physician will see hypersomnia patients from time to time. I’ve been doing this since 1992, and you sometimes run into patients like this: They’re fairly young, but they’re just addicted to sleep. They sleep for long periods of time, and they’re very efficient sleepers – they tend to sleep deep, and they can sleep through alarms and fires and sometimes even bombs. But despite sleeping all that time, they wake up very unrefreshed and they’re still sleepy during the day.

BT: And you’ve pointed out that this pattern is different from what we see in narcolepsy.

DR: Hypersomnia has been labeled with so many inappropriate names, and “narcolepsy” is the biggest one we hear. But narcolepsy has been classified very precisely into several categories – for instance, Type I narcolepsy, which is characterized by the loss of this neuropeptide chemical known as hypocretin. And narcolepsy – the literal translation is “to be seized by sleep.” Narcoleptics don’t actually sleep more than healthy people over an average 24-hour period; their disorder is characterized by sudden attacks of sleepiness. So to characterize a person with hypersomnia as “narcoleptic” is really a disservice to the language.

BT: What are some unique features of hypersomnia?

DR: Hypersomnia patients don’t really respond to traditional stimulants – they can still sleep for hours even after taking a large dose of caffeine, or an amphetamine. And what they usually describe is that these stimulants make them feel physically awake, but they never quite wake up mentally – they feel as if they’re in a fog. Academics at sleep centers around the country agree that they’ve seen these patients, but no one knew exactly how to treat them.

BT: Could there be such a thing as “hypersomnia with narcoleptic symptoms,” or are these two disorders completely distinct?

DR: I think it’s closer to the former, which makes the process of diagnosing these disorders even more confusing. There are people who are labeled “narcoleptic” because they fall asleep during the day and go right into a dream – and this is characteristic of the “genuine” narcolepsy I was just mentioning. But in reality, recent research has found that many narcoleptics are more like our hypersomnia patients – they sleep for long periods of time during the day.

BT: So how do you distinguish these diagnoses in the clinic?

DR: Well, see, that’s what makes this even trickier: Patients don’t come into a clinic complaining that they fall directly into dream states – that’s just not a complaint you’d hear. So my question is, why are we classifying patients as “narcoleptic” based on whether or not they fall into a dream state when they have a nap during the day? As physicians, we start diagnosing a new disorder based on clusters of signs and symptoms, rather than on underlying biological processes – but as time goes by and we come to better understand the biological basis for a particular disorder, we update our diagnostic criteria so we can more accurately categorize the patients we see. And that’s been a huge uphill battle for these sleep disorders, because we’re only beginning to understand their biochemical causes.

BT: Do we have any idea, neurochemically, why hypersomnia symptoms are so unusual?

DR: I think we’re putting our finger on it with this research. The traditional approach is sort of a “Western” approach – what I mean is, when Western neuroscience deals with a problem, we have a bias to characterize the problem as “something’s missing.” In this case, that plays out as, “This patient’s wake-up system isn’t working properly,” so we say, “Give it more stuff to make it awake.”

BT: But that’s focusing on the wrong issue.

DR: Right. By analogy, we’re pushing the accelerator pedal – but the problem isn’t that we need more gas; it’s that the parking brake is still on. The “parking brake” is gamma-aminobutyric acid (GABA), which is an inhibitory neurotransmitter chemical that helps promote sleep. And that parking brake needs to be disengaged before we can hit the gas and hope to actually get moving.

BT: And in this study, you looked at substances that interact with GABA receptors, and isolated a chemical that’s strongly correlated with hypersomnia.

DR: Exactly. We’ve characterized this chemical quite well – in fact, when we submitted our paper to the New England Journal of Medicine, they told us they were impressed with the level of detail in our pharmacological analysis of this chemical’s interaction with GABA receptors. The real question now is, is this biological agent unique to the types of hypersomnia we studied, or might it also be a factor in other known types of narcolepsy that we didn’t look at? Or might it be part of a general-purpose pathway to sleepiness, common to all human brains? That’s actually the explanation we’re leaning toward, though you can’t make that claim from our data in this particular paper.

BT: There’s been a lot of media blitz around this study since you announced your results. Why do you think this work resonates so strongly with the general public?

DR: I think it speaks, first of all, to our culture’s traditional and literary fascination with sleep. There’s Sleeping Beauty, Rip Van Winkle – for centuries, we’ve been enamored with stories of people who sleep for long periods of time. It’s also the opposite side of the coin of insomnia, which is something a lot of us struggle with. When I talk to reporters about hypersomnia, one comment I hear a lot is, “Can you give me a dose of that?” They’re jealous! So I think it speaks to a lot of topics that puzzle and intrigue us.

BT: It sounds like people find the actual experience of hypersomnia difficult to relate to, even if they’re jealous of it.

DR: And yet, what our data really seem to suggest is that hypersomnia is just one end of a spectrum – a bell curve – that includes all of us. The majority of us sleep for seven and a half, eight hours – and what we’re showing here is that even people who need to sleep nine or ten hours are probably just less extreme variants from the center of that curve. So my wife and I joke that we can definitely relate to this – when her family come to visit for the holidays, they can sleep for nine hours and take a two-hour nap in the afternoon.

BT: So this data could give us insight into why some people are fine with six hours of sleep, while others are drowsy if they get less than nine.

DR: I think that’s the point. Beyond the direct implications of being able to treat hypersomnia, we’re getting some good insights into how normal sleep is generated – and maybe even why we need to sleep at all.

BT: That question’s always intrigued me – it’s definitely one of the all-time great science mysteries.

DR: Well, if we know what this molecule is, and what chemical pathways it’s involved in, and we can make specific statements like, “It accumulates in excess under these certain conditions,” I think we’re gonna be pretty damn close to understanding why we sleep.

BT: That’ll be really interesting to see. I’m excited to hear about where that research goes.

DR: We’ve actually gathered quite a bit of sleep-related data that didn’t make it into this paper, so we’ll be publishing more about our findings in the near future. So stay tuned.

I definitely will, and I’ll do my best to keep all of you in the loop, too. Thanks for joining us – we’ve got lots more exciting interviews coming up soon!


Science Fights Back With Open Access

A major paradigm shift is taking the science world by storm. Open source is taking over.

For more than a century, scientists have depended on peer-reviewed journals to keep them up to date on the latest research. But as many of these journals have raised their subscription fees to bank-breaking levels, and locked life-saving research behind exorbitant paywalls, the gloves are finally coming off. Thousands of researchers are fighting back by boycotting publishers, submitting their papers to open-access journals like PLOS ONE and PNAS, and – most excitingly of all – making their datasets freely available online, for everyone.

As of September 2012, PLOS ONE appears to be the biggest scientific journal in the world.

But that’s just the beginning. In October 2012, an international team of neuroscientists known as the CONNECT Consortium released the first micro-structure atlas of the human brain: A massive open-access database of brain connectivity down to the micron scale. Quite a bit of their data is already available on their website, to be used with free open-source brain imaging programs like OpenWalnut and BrainVISA. Anyone with a computer and a willingness to tinker can play with the same data that professional neuroscientists are using.

Once upon a time, this guy was just a geek who liked to tinker.

The CONNECT project has already led to dozens of breakthroughs, including more precise techniques for modeling white matter wiring, advanced technologies for preserving live samples of neural tissue, and more than 80 new peer-reviewed journal papers based on the data the project assembled. And the work continues today – the team plans to continue gathering data, refining their techniques, and releasing new tools and models to scientists and the public.

The CONNECT Consortium aren’t the only ones with this dream. The Human Connectome Project, which ultimately aims to simulate the functioning of an entire human brain, makes intricate reconstructions of brain functionality available to anyone who qualifies for an account. If you’re in the mood for instant access, the Open Connectome Project will let you explore the brains of various animals online, right now. also has loads of models for you to play with.

If you’d rather gather your own data, grab a $299 neuroheadset and check out OpenVIBE, a free open-source program that helps you record your brainwaves, design your own experiments, and even create video games and art projects controlled by your brain activity. Though the EEG recordings you’ll get with a neuroheadset aren’t as deep or precise as the fMRI and DTI data used in many imaging studies, plenty of modern research is still EEG-based. It’s all about choosing the right tool for the right experiment.

What is a scientist, really? Anyone who’s willing to dig into the data, test expectations, and revise conclusions when they don’t agree with reality. If you agree that it’s more important to be true to the facts than to win an argument, you’re already a scientist at heart.

It’s like in the old quote attributed to the Buddha:

Do not believe in anything simply because you have heard it… But after observation and analysis, when you find that anything agrees with reason and is conducive to the good and benefit of one and all, then accept it and live up to it.

Every day, the world is metamorphosing. The landscape of science is shifting and quaking. Have you ever dreamed of making a scientific discovery? What’s stopping you?

brain comp chip SS

Q&A: Can We Preserve Our Brains After Death?

As promised, here’s the first-ever official Connectome Q&A! We’ve been getting lots of incoming questions on our Facebook and Twitter pages – some of them on the technical side; others of the more “general interest” variety. Most of these questions require pretty involved answers – and it’s important to me that each of them gets the full treatment it deserves.

So for today’s Q&A, I’ve decided to focus on just one question. That doesn’t mean we’ve forgotten the others, though – we keep everything archived, and we’ll be doing plenty more Q&As in the future. So keep sending those neuroscience queries and article requests our way.

And now, let’s get into today’s question!     —Ben


Q. “What is the best current method to preserve a connectome or whole brain – cryonics, vitrification, chemical brain preservation or something else?”     Ivan Smirnov, via Facebook


A. There are actually two different questions here: 1) “What’s the best way to preserve a brain?” and 2) “What’s the best way to preserve all the information in a brain?” There’s also a third question that’s sorta implied by the first two: “Is it possible to preserve a person’s ‘self’ by preserving that person’s connectome?” Let’s take these questions one-by-one.

When it comes to preserving brain tissue, the most successful and widely used technique available today is cryopreservation: cooling a brain to sub-zero temperatures, which stops all biological processes. Techniques like slow programmable freezing (SPF), along with cryoprotectant chemicals, can protect cells from being damaged by freezing. In fact, laboratories around the world use CPF and cryoprotectants to preserve living cells and organs – and even whole animals – for later resurrection.

A technique that shows some promise for the near future is neurovitrification, which transforms the water in living neural issue into a glass-like solid, allowing cells to be frozen with minimal damage. Though vitrification preserves many organs quite well, we’re still years away from being able to freeze and resurrect a mammalian brain – let alone a human one. In theory, a perfected neurovitrification technique would preserve living neurons right down to the molecular level, locking every atom of every synapse in place.

That kind of lockdown would be crucial for preserving and resurrecting a brain, because most information in the brain is stored not in physical connections, but in electrochemical communication networks that shift and morph from moment to moment. Keeping those synaptic molecules in place would be the only way to resurrect a brain without “wiping its hard drive.” For the same reason, it’d be vital (no pun intended) to preserve a brain before its owner had died; once those neurons have stopped firing, most of the brain’s stored information is lost forever.

Early brain preservation experiments didn’t always go as planned. (image credit:

This brings us to another approach: preserving the information encoded in a brain’s connectome. The idea here is that if we can understand precisely how the brain encodes various kinds of information, we could record and save a digital “copy” of its connectome – perhaps without having to map the location of every molecule in every synapse – and, helpfully, without having to freeze a living person (possibly ending his/her life and thus defeating the whole point).

To understand how a connectome does what it does, efforts like the Human Connectome Project, the Whole Brain Catalog and the Open Connectome Project aim to produce functional simulations of brain activity at all scales. Before we can build a digital copy of a connectome, we need to understand exactly what needs to be copied, and how it’s supposed to work.

Connectome naysayers claim that even this won’t be enough. They draw comparisons between the Human Connectome Project and its earlier cousin, the Human Genome Project (HGP). Although the HGP has led to plenty of breakthroughs, we’re still a long way from understanding what most of our genes actually do. And whereas a human genome has about 3,000,000,000 (3 billion) base pairs, a human connectome may involve as many as 100,000,000,000,000 (one hundred trillion) synaptic connections – all of them constantly transforming and exchanging information with their neighbors. At the very least, we’re going to need some major innovations in computing power, and a vastly expanded program of data-gathering, before we can simulate an entire human connectome at the synaptic level.

Of course, none of this tells us anything about whether preserving a person’s connectome or brain – even flawlessly – will preserve that person’s mind/self/individuality. Sebastian Seung, one of the big brains behind the Human Connectome Project, has called the question of immortality “the only truly interesting problem in science and technology.”

We know that some animals, such as frogs and salamanders, can be frozen for long periods, thawed, and awakened to keep going about their amphibian business. So far, though, no one’s been able to do this with a mammal – so it’s unclear whether it’d be possible to resurrect your dog or cat, spunky personality and all. (Unsurprisingly, that hasn’t stopped wealthy pet owners from putting Rover on ice just in case.)

As with the connectome mapping projects, the problem with preserving a personality is that no one knows exactly what needs to be preserved: living nerve cells, positions of neurotransmitter molecules, and/or certain kinds of neurochemically encoded data might all be necessary pieces of the puzzle.

In other words, what works for frogs and salamanders may or may not work for mammals like us. It’s unclear whether what we call a “self” is correlated with stable body temperature, or even with a cerebral cortex – for example, there’s some evidence that octopi may have a form of self-awareness, and they’re ectothermic and have very different neural wiring from vertebrates.

It’s also very unlikely that one day in vertebrate evolution, the “self” just popped into being – more likely, self-awareness arose gradually out of the interactions among many self-referential circuits of brain activity; the same goes for personalities, emotions, hopes, fears, and all the other vaguely defined ghosts that haunt our machinery.

What this implies is that the processes of understanding, disassembling and reverse-engineering the “self” are going to be very gradual ones. It’s likely that we’ll spend decades studying correlations between neural activity and subjective experience before we understand exactly how they correlate – which means that for the foreseeable future, the only one who’ll know for certain whether a resurrected brain contains “the true-blue you” will be …well… you.

Matt Wall

Brain Scans and Bold Plans: Our Interview with Matt Wall

Sometimes, a conversation takes you to places you never would’ve expected. Matt Wall and I struck up a chat about brain-scanning technology early this year, and he mentioned that he’d like to do an interview for The Connectome.

Since he’s got 5+ years of published brain research under his belt, I jumped at the chance.

I figured we’d be talking about what life’s like in an fMRI lab, and maybe about some recent discoveries – but we wound up chatting about science misconceptions, the nature of pain, post-traumatic stress disorder and psychedelic drug trips (among other things). I think you’ll enjoy hearing his insights as much as I enjoyed picking his brain.    –Ben

Ben Thomas:
So, Matt, how’d you get involved in fMRI research?
Matt Wall: My bachelor’s degree was actually in psychology. I earned my Ph.D. in Cambridge, and I started working with fMRI in my post-doctoral work – first in a vision lab, looking at low-level visual physiology, and then working on the spinal cord. So I keep getting further and further away from my roots as a psychologist.
BT: And you’ve done some work in cognitive neuroscience as well. So, quite a broad range of topics. What’s the unifying theme in all this work?
MW: Well, in a sense, I’ve just been moving from one field to another as I find interesting projects – but the unifying theme is really the fMRI itself. I’ve come away from each of these projects with a richer understanding of the technology. fMRI is such a technical specialty that it often takes years to become familiar enough with the technology to understand how to perform effective research with it. Once you’ve got that understanding, though, you can apply it to studying lots of different areas of neuroscience.
BT: Once you’ve reached that level of familiarity, what kinds of tasks are you expected to be involved in? What’s day-to-day life like in an fMRI lab?
MW: My latest project has been studying reactions to pain – so a lot of my day-to-day work has been strapping electrodes to people’s heads, giving them electrical shocks, and recording their brain activity. Which sounds pretty sadistic, but we’re doing it for a good reason: We’re particularly interested in the trigeminal nerve, and its role in processing pain signals. Although this nerve is technically part of the peripheral nervous system, you can – in theory – get BOLD (blood oxygen level-dependent) fMRI signals from it, as you can from, say, the cerebral cortex. Our goal has been to try to figure out where exactly in the pain system a given drug starts messing with the signal. We haven’t quite managed to get things working as we’d hoped, though, and my contract with that lab is about to be up. But it’s been an interesting project to work on.
BT: To backtrack just a bit, you mentioned looking for BOLD signals, which is a great opportunity to talk about a common source of confusion I see in articles on brain studies: fMRI doesn’t directly measure neural activity at all.
MW: Right. What fMRI is actually tracking is the ratio of oxygenated to deoxygenated hemoglobin in a given area – basically, the oxygen level in the blood pumping through that region of the brain. One thing we know about the brain’s vascular system is that it tends to overcompensate; so the more active a certain area of the brain becomes, the more oxygen it demands, and the more oxygen the vascular system dumps into it.
BT: So fMRI is measuring the level of oxygen in that area, but not what that area’s doing – it could be processing input from some other area; it could be sending out excitatory or inhibitory signals, or a mixture of the two…
MW: That’s one of the trickiest things about analyzing fMRI data. You’re comparing brain activity during a task with “control” activity – i.e., activity in that same area when that task isn’t being performed – and sometimes you notice an increase in activity in a certain region during the task, while maybe you notice a decrease in others; they were more active in the control condition. So there’s often the possibility that an increase of activity in one area could mean it’s inhibiting activity in another. But it’s very difficult to be sure about those kinds of causal interpretations.
BT: And yet every day we’re reading headlines like, “Brain Area Responsible for [X] Discovered!” All we really know is that’s an area that becomes more active during task [X]. It could be processing that task, or it could be inhibiting another region that interferes with the task.
MW: A better way to phrase it would be, “Brain Area Associated with [X] Discovered.” It’s quite a leap to say that activity in a certain area is directly causing a certain effect – especially if that supposed effect is something as complex as a whole behavior or a personality trait.
BT: Yeah, no kidding. So, now that this pain research is wrapping up, what’s on the horizon for you?
MW: Lately I’ve been getting into neuropharmacology. I recently wrapped up some work for GlaxoSmithKline, at a lab that was studying pharmaceutical drugs before they went to market. But my most recent project has actually been a TV series exploring the effects of recreational drugs on the brain. I was just a relatively small part of a large team working on the program – the major players were Prof. David Nutt of Imperial College and Prof. Val Curran of UCL, with Dr Robin Carhartt-Harris being the principal investigator. Most recently we performed fMRI scans on people who were on quite large doses of MDMA (ecstasy). So that’s been fun.
BT: Any interesting discoveries yet?
MW: A few things, actually; yeah. The point of the MDMA episode was to examine the therapeutic uses of that drug. MDMA was used in clinical settings quite a lot in the 1940s, when it was first discovered – but once it became known as a street drug, all that research stopped, and a lot of misinformation started spreading.
BT: The claims that it caused “holes in the brain” and all that.
MW: Right. But there’s some evidence that MDMA can be used to help treat PTSD (post-traumatic stress disorder). A therapist can walk patients through memories of their traumatic experiences while they’re on ecstasy; they’re still lucid about the details of the memory, but the drug seems to counteract a lot of the agitation and distress they’d normally feel. So after a few walkthroughs of the traumatic memory while on MDMA, the patients develop the ability to think through the details of the experience without suffering that intense anxiety.
BT: And what’s fMRI telling you about how that works neurologically?
MW: What we’re finding so far is that MDMA usage is correlated with increased activity in the visual cortex (vs. placebo) during recall of emotionally positive memories. And that lines up with our subjects’ reports – they generally report that those memories are much more vivid than usual when they’re on MDMA. And during recall of emotionally negative memories, we’re seeing that MDMA use is correlated with much lower activity in the parahippocampal gyrus, which is involved in memory retrieval, and in the amygdala, which is associated with negative emotions like fear and disgust. So it’s possible that MDMA inhibits the negative emotions associated with those memories.
BT: Sounds like MDMA shows some promise for clinical treatment.
MW: I think that’s likely. Oh, and there was also another episode where we were studying the effects of psilocybin, the chemical in “magic mushrooms.” I took part in that one myself, which was quite interesting. It was a crazy experience, actually. A real roller coaster.
BT: The last time a lot of these drugs were seriously studied was back in the ’60s, when they were still legal. And back in those days, we didn’t have fMRI; we had EEG (electroencephalography), which really just measures electrical activity across the scalp. So I’m really excited to see what we’ll discover now that we can correlate activity in a specific brain region with all these perceptual distortions and expansions that psychedelic drug users describe.
MW: I think the tide of public opinion is starting to shift. MDMA, psilocybin, LSD, and so on are really powerful mind-altering compounds. There’s a lot of anecdotal evidence about them; and so far, only a few studies demonstrating that, say, psilocybin can alleviate depression in people who aren’t responsive to other treatments. These are very small studies; it’s tough to get bigger funding and wider sample groups, because, as you say, these drugs are still illegal in many parts of the world. But over the past few years, I’m hearing more and more researchers saying, “Hey, if these drugs have potential therapeutic benefits, we really should be investigating them further.” Any powerful mind-altering compound carries certain risks, of course – but there’s no reason they shouldn’t be tested in clinical environments.
BT: Absolutely. This sounds like a fascinating project; when I asked you to talk with me about fMRI research, I had no idea we’d wind up talking about psychedelic drug trips.
MW: Yeah; it’ll be interesting to see where this research takes us.
Thanks again, Matt, for taking the time to chat. We’ve got more interviews with big names in neuroscience on the way, so stay tuned for lots more exciting times!




S. Emmons

“Using Worms to Crack the Human Brain” — Podcast 4: Scott Emmons

On episode 4 of the Connectome podcast, I chat with Scott W. Emmons, Ph.D., a professor of neuroscience and genetics at Albert Einstein College of Medicine. Dr. Emmons talks about his cutting-edge connectomics research, which may help us understand how neural circuits “decide” on a particular behavior. Though his recent work focuses on the nervous systems of microscopic worms, its implications may reach all the way to the human brain.


Click here to play or download:

Enjoy, and feel free to email us questions and suggestions for next time!


(Produced by Devin O’Neill at The Armageddon Club)


The Lurking Lizard

He has haunted us for more than fifty years – this strange scientist, with his theory of primal reptiles embedded in each of us. And for years I wondered, Could this bizarre hypothesis be true? Might it explain the ancient instincts – so contrary to my intentions – which I felt arising from the depths of my unconscious mind? Could it really be possible that inside my primate brain lurked a vicious lizard mind, a relic from the era when reptiles ruled the earth?

As it turns out… no, actually. The theory – if not the man who coined it – has proven outright insane in light of the latest scientific research. And yet, speakers and writers around the globe continue to trumpet the truth of the idea.

Let me lay the facts bare for you, and explain the enduring appeal of this weird  theory, in my latest article for Scientific American: “Revenge of the Lizard Brain!”

“There’s a scene in Fear & Loathing in Las Vegas in which the writer, high out of his mind on hallucinogens, watches a roomful of casino patrons transform into giant lizards and lunge at each other in bloody combat. Under the veneer of civilization, the scene suggests, we’re all still reptiles, just waiting for the moment to strike.

Like the Fear & Loathing scene, the Triune Brain idea holds a certain allegorical appeal: The primal lizard – a sort of ancestral trickster god – lurking within each of us. But today, writers and speakers are dredging up the corpse of this old theory, dressing it with some smart-sounding jargon, and parading it around as if it’s scientific fact…”


The Listeners from Below

Deep within your brain, they are listening. In still silence, they await signals from afar – dim echoes of distant calls. And when they hear what they’ve been waiting for… they will awaken.

They are known as neural stem cells – and not only are they real; researchers have just made some major discoveries about how they work. Those discoveries demonstrate that what seems like a biological accident may in fact be a crucial component of a delicate process.

Let me tell you the tale, in my new article for Scientific American: “What Your Neural Stem Cells Aren’t Telling You.”

In 2000, a team of neuroscientists put an unusual idea to the test. Stress and depression, they knew, made neurons wither and die – particularly in the hippocampus, a brain area crucial for memory. So the researchers put some stressed-out rats on an antidepressant regimen, hoping the mood boost might protect some of those hippocampal neurons. When they checked in a few weeks later, though, the team found that rats’ hippocampuses hadn’t just survived intact; they’d grown whole new neurons – bundles of them. But that was only the beginning…

Chemistry woman

Brains and Brilliance

Where in the brain, exactly, is intelligence? Is a high I.Q. just a result of a flawed test – or do high-I.Q. brains have specific, measurable differences from others? Answers await, Intrepid Reader – but first we have to make sure we’re asking the right questions.

Let’s start with the big news: a study just published in the Journal of Neuroscience reports that when a certain area of the frontal lobe has unusually wide and active connectivity, a higher I.Q. tends to follow. The trouble is, though, that a high I.Q. only reflects certain types of mental abilities – so what this discovery really means is that a certain functional network in the brain plays a major role in certain kinds of smart thinking.

In fact, it makes perfect sense that the brain region we’re talking about here – the left lateral prefrontal cortex (lPFC) – would be central to the kinds of thought processes that earn you high I.Q. scores: namely, arranging logical steps and figuring out abstract rules. The wider and stronger the lPFC’s connections are, the more neural processes it can involve in its orderly calculations. And yet, while there’s no doubt that those calculations are some of the human brain’s most powerful and effective abilities, they’re only a few of the many skills we recognize as “intelligent.”

The limitations of I.Q. tests are rooted in the 19th century, when British and American scientists began developing the first intelligence tests. In those days, a commonly accepted assumption was that people of European descent had the highest intelligence on earth – so, naturally enough, researchers came up with tests on which well-educated Westerners tended to score the highest. And this might all just be an embarrassing historical footnote – except that today’s I.Q. tests still produce racially and culturally biased results.

The left lateral prefrontal cortex puts on an awesome laser light show for the whole brain.

What’s more, the reasons for those biases aren’t always clear-cut: a person’s individual attitudes about tests, school, and intelligence may influence his or her score as much as any cultural bias in the test questions. (Having grown up in a small town in West Texas, I know firsthand how it feels to be pressured to hide your intellect – even to be ashamed of it.)

Meanwhile, studies have found that it’s fairly easy to “outsmart” an I.Q. test – to teach students tricks and tactics for achieving high scores. This would seem to imply either 1) that a few weeks of practice drills can significantly raise a person’s intelligence, or 2) that the test is just measuring proficiency in a specific set of teachable skills.

In the later half of the 20th century, researchers like David Wechsler tried to expand the range of I.Q. tests, developing much more precise metrics for assessing verbal skills, spatial reasoning, ability to identify patterns, and so on. But by the early 1980s, researchers like Howard Gardner were insisting that some kinds of intelligence – and, in fact, many aspects of what we call “genius” – simply can’t be measured with a system like I.Q. assessment.

Gardner’s theory of “multiple intelligences” distinguishes linguistic and logical types of intelligence – the types that result in high I.Q. scores – from types like musical intelligence (the ability to recognize and compose pitch and rhythm) and intrapersonal intelligence (the ability to understand one’s own motivations and feelings).

Today, though, researchers have narrowed the field down to two intelligences: fluid intelligence (the ability to solve problems in novel situations) and crystallized intelligence (the ability to remember facts and use specific skills). Even so, it’s clear that intelligence isn’t just one attribute, but an interrelated collection of traits.

So when this new study’s co-author, Todd Braver, explains his team’s results, he’s careful not to overstate his case:

Part of what it means to be intelligent is having a lateral prefrontal cortex that does its job well; and part of what that means is that it can effectively communicate with the rest of the brain.

In other words, a well-connected lPFC is a handy thing to have, but it’s just one aspect of intelligence. It’s definitely got its benefits – it keeps you open-minded, and it may even help you stick to a healthier diet. On the other hand, it also makes you more likely to experience anxiety and depression, to develop schizophrenia, to enjoy drugs (especially psychotropics), and to suffer all kinds of expectation frustration. The upside of all these discoveries, though, is that the better we understand this lPFC network, the more precisely we’ll be able to diagnose and treat these kinds of troubles.

As you can see, intelligence (in all its many-splendored forms) isn’t exactly a process or a trait – it’s more a way of connecting; of assembling disparate thoughts, feelings and ideas into Gestalts: wholes that become more than the mere sum of their parts. That connectivity can be both a blessing and a curse – but in any case, it’s one of the core reasons your brain can conceive such strange and unique ideas as art and language – and even turn inward and contemplate itself.


Memories on a Microchip

Are your memories real? How do you know?

These sound like questions from a mind-bending thriller – Total Recall, say; or Inception. But this isn’t science fiction. Researchers around the world are implanting memories, turning them on and off – and, according to one team, storing them on microchips.

Wow. Okay. Let’s back up here.

Memories, as it turns out, aren’t the most stable things in the world. Our long-term memories are more like scripts for plays than files on a hard drive – and with each new performance, details change. In fact, our brains can easily rewrite our memories to fit with the socially accepted versions of events – we don’t even seem to notice the difference.

Colin Farrell suddenly forgets which room of the maze contains his delicious cheese.

All of which is weird, to be sure. But it gets weirder.

In 2011, researchers at Wake Forest University and the University of Southern California developed “memory chips” that can be used to turn specific memories on and off in a mouse’s brain. With the flick of a switch, a mouse forgets all he knows about how to navigate a maze – and with a flick in the other direction, the little guy recalls everything in a sudden flash of insight.

And in early 2012, scientists at the Scripps Research Institute electronically inserted memories into the brains of mice. In other words, they figured out which specific neurons in a mouse’s brain fire when it recognizes a familiar place – then they inserted a microchip that artificially stimulated those same neurons to fire as the mouse walked into an unfamiliar room.

This resulted in something deeply bizarre:

When an ensemble of neurons for one context (ctxA) was artificially activated during conditioning in a distinct second context (ctxB), mice formed a hybrid memory representation.

In other words, the mice instantly formed a memory of a place they’d never seen before: an artificial hybrid memory. No suit-clad agents or Edith Piaf songs needed. But even that isn’t the really weird part. Are you ready for the really weird part?

The scientists took their memory microchip and put it into another mouse’s brain – and that mouse apparently experienced the same hybrid memories.

Could technology like this be used to restore memory in brain-damaged patients? Could it disarm the emotional pain of a traumatic memory, while leaving the recollection itself intact? Would saving our memories digitally help preserve their original accuracy?

As you can imagine, questions like these have sparked a riot of blog posts declaring that The Matrix is upon us, thought control is now a reality, whole memories and learned behaviors can be transferred from one brain to another – you get the drift. If you want to call a simple “recognition alert” a full-fledged memory… be my guest, I guess – but I want to see what happens when other labs try to replicate this experiment; in particular, I want to see how more complex brains respond.

Most of all, though, I feel a war churning within me when I think about testing this technology on humans. Half of me hopes it doesn’t work at all, and half of me wants to be first in line to try it out. I yearn to understand it from the inside, subjectively; to know how it feels to believe a true falsehood; to examine the memories that compose my “self,” and to see for myself just how fragile it is.

All of which is, of course, terrifying. Which is exactly why it fascinates me.


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