In a lab at Stanford University, a mouse is showing signs of depression. For around 10 weeks, it has experienced a series of irritations, from bouts without food or water, to erratic sleep patterns. Now, its motivation is low—when picked up by the tail, it makes few attempts to escape, and it doesn’t try to explore new spaces. It’s also less willing to sip from a sugary liquid– a sign that it gets less pleasure from normally pleasurable activities. It is never easy to assess the mental health of an animal, but this mouse is clearly showing some of the classic symptoms of depression.
But not for long.
Earlier, Kay Tye and Julie Mirzabekov altered the mouse so that a flash of light can activate a small part of its brain—the ventral tegmental area (VTA), near the bottom of the brain and close to the midline. A burst of light, and the mouse’s behaviour changes almost instantly. It struggles when held aloft, it explores open areas, and it regains its sweet tooth. A burst of light, and its symptoms disappear.
But on the other side of the country, at the Mount Sinai School of Medicine, Dipesh Chaudhury and Jessica Walsh are doing the same thing to completely different effect. Their mice have been altered in a similar way, so that light can also switch on their VTA neurons. But these rodents have endured a shorter but more intense form of stress—10 days of being placed in cages with dominant, aggressive rivals. Because of the resulting attacks, some of them have developed depressive symptoms. Others are more resilient. But when Chaudhury and Walsh flashed the VTAs of these mice, resilient individuals transformed into susceptible ones.
Both studies used the same methods to trigger neurons in the same part of the brain… and got completely different effects. In Tye and Mirzabekov’s experiment, depressed mice resumed their normal behaviour. In Chaudhury and Walsh’s study, the resilient mice showed more depressed symptoms.
There have been many attempts to create a virtual brain, by simulating massive networks of neurons. But brains aren’t just piles of neurons. They also do things. They perceive. They reason. They solve tasks. Enter Spaun – the first brain simulation that actually shows simple behaviour, from recognising and copying a number, to solving simple reasoning problems.
It simulates 2.5 million virtual neurons, including the electricity that course through them, and the signalling chemicals that pass between them. It’s almost as accurate as the average humans at 8 separate tasks and, rather delightfully, reproduces many of our strange quirks – like the tendency to remember items at the start and end of a list.
I’ve written about Spaun for Nature News. Head over there for more
But neurons don’t always need synapses to communicate—some in the antennae of a fly can influence one another without any direct connections. The electric field produced by one can silence its neighbour, like two individuals standing side by side and whispering “Sssssshhhh” at each other.
This phenomenon, known as ephaptic coupling, has been discussed for a long time but it’s always been a bit obscure and arcane. There are very few examples of it, and none where this indirect silencing actually affects an animal’s behaviour. Su has changed that – his study shows that ephaptic coupling affects a fly’s or mosquito’s sense of smell. That knowledge might be useful for protecting crops from hungry insects, or people from disease-carrying ones.
I’ve written about this story for The Scientist, so head over there for more details.
Image by Martin Hauser
Meet Laurax, a not-very-bold, not-that-exciting new fragrance. According to a panel of sniffers, it’s neither appealing nor revolting. It’s “intermediately pleasant”. People almost trip over themselves to describe it in non-descript terms—“fragrant”, “chemical” and “perfumery”.
Laurax isn’t going to set the perfume world ablaze in the near future, but its scientific implications are fascinating. This bizarre scent is actually a set of completely different fragrances that all smell roughly the same. It’s the odour version of “white”.
The colour that we call white is a blend of many different wavelengths of light. Add red and blue light together, and you get magenta. Add other colours and eventually, you converge on white. The same applies to sounds: if you combine tones of different frequencies, you eventually arrive at a perceptual hum called “white noise”. There’s no fixed formula for making white light or white noise. You don’t need to mix a specific set of colours or frequencies. As long as the individual ingredients are different enough, and roughly equal in intensity, whiteness emerges.
This post contains material from an older one, updated based on new discoveries.
There are many things you don’t want gathering in large numbers, including locusts, rioters, and brain proteins. Our nerve cells contain many proteins that typically live in solitude, but occasionally gather in their thousands to form large insoluble clumps. These clumps can be disastrous. They can wreck neurons, preventing them from firing normally and eventually killing them.
Such clumps are the hallmarks of many brain diseases. The neurons of Alzheimer’s patients are riddled with tangles of a protein called tau. Those of Parkinson’s patients contain bundles, or fibrils, of another protein called alpha-synuclein. The fibrils gather into even larger clumps called Lewy bodies.
Now, Virginia Lee from the University of Pennsylvania School of Medicine has confirmed that the alpha-synuclein fibrils can spread through the brains of mice. As they spread, they corrupt local proteins and gather them into fresh Lewy bodies, behaving like gangs that travel from town to town, inciting locals into forming their own angry mobs. And as these mobs spread through the mouse brains, they reproduce two of the classic features of Parkinson’s disease: the death of neurons that produce dopamine, and movement problems.
This is the clearest evidence yet that alpha-synuclein can behave like prions, the proteins that cause mad cow disease, scrapie and Creutzfeld-Jacob disease (CJD). Prions are also misshapen proteins that convert the shape of normal peers. But there is a crucial distinction: prions are infectious. They don’t just spread from cell to cell, but from individual to individual. As far as we know, alpha-synuclein can’t do that.
Alan Kingstone, a psychologist at the University of British Columbia, had a problem: all humans have their eyes in the middle of their faces, and there’s nothing that Kingstone could do about it. His 12-year-old son, Julian Levy, had the solution: monsters. While some monsters are basically humanoid in shape, others have eyes on their hands, tails, tentacles and other unnatural body parts. Perfect. Kingstone would use monsters. And Julian would get his first publication in a journal from the Royal Society, one of the world’s most august scientific institutions.
In 1998, Kingstone showed that people will automatically look where other people are looking. Other scientists have since found this gaze-copying behaviour among many other animals, from birds to goats to dolphins. It seems fairly obvious why we would do this—we get an easy clue about interesting information in the world around us. But what are we actually doing?
There are two competing answers. The obvious one is that we’re naturally drawn to people’s eyes, so we’ll automatically register where they’re looking. Indeed, one part of the brain – the superior temporal sulcus – is involved in processing the direction of gazes. The equally plausible alternative is that we’re focused more broadly on faces, and the eyes just happen to be in the middle. After all, we see faces in inanimate objects, and we have a area in our brains—the fusiform face area (FFA)—that responds to the sight of faces.
One evening, Kingstone was explaining these two hypotheses to Julian over dinner. “A colleague had said that dissociating the two ideas — eyes vs. centre of head — would be impossible because the eyes of humans are in the centre of the head,” Kingstone said. “I told Julian that when people say something is impossible, they sometimes tell you more about themselves than anything.”
Julian agreed. He thought it would be easy to discriminate between the two ideas: just use the Monster Manual. This book will be delightfully familiar to a certain brand of geek. It’s the Bible of fictional beasties that accompanied the popular dice-rolling role-playing game Dungeons and Dragons. Regularly updated, it bursts with great visuals and bizarrely detailed accounts of unnatural history. It has differently coloured dragons, undead, beholders… I think one edition had a were-badger. Parts of this blog are essentially a non-fictional version of the Monster Manual.
In a lab at MIT, a rat enters a T-shaped maze, hears a tone, and runs down the left arm towards a piece of chocolate. It’s a habit. The rat has done the same thing over so many days that once it hears the tone, it’ll run in the same direction even if there’s no chocolate to be found. Humans are driven by similar habits. Every morning, I hear my alarm go off, put some clothes on, and shamble into the kitchen to brew some coffee.
Habits, by their very nature, seem permanent, stable, automatic. But they are not, and the MIT rat tells us why. Earlier, Kyle Smith had added a light-sensitive protein to one small part of its brain – the infralimbic cortex (ILC). This addition allows Smith to silence the neurons in this one area with a flash of yellow light, delivered to the rat’s brain via an optic fibre. The light flashes for just three seconds, and the habit disappears. The rat hears the tone, but no longer heads down the chocolate arm.
The experiment shows that even though habits seem automatic, they still depend on ongoing supervision from the ILC and possibly other parts of the brain. They’re ingrained and durable, but subject to second-by-second control. And they can be disrupted in surprisingly quick and simple ways.
“We were all stunned by how immediate and on-line these effects really are,” says Smith. “Changing the activity of this small cortex area could profoundly change how habitual behaviour was, in a matter of seconds.”
Last Wednesday, Nobel laureate Daniel Kahneman sent an email to a group of a dozen or so psychologists telling them that the credibility of their field was in danger. The recipients all worked on social priming – the study of how subtle unconscious cues can influence our behaviour. It’s an area that has attracted controversy of late, due to failed replications of classic results, the outing of fraudulent researchers, and a more general concern among psychologists about the validity of their field’s results.
Kahneman meant the email as helpful advice, but his wording couldn’t have been stronger: “Your field is now the poster child for doubts about the integrity of psychological research… I believe that you should collectively do something about this mess.” His solution: a “daisy chain” of replications, where laboratories collaborate to check the results of their neighbours, in an open, transparent, and pre-established way.
Kahneman requested that the email be sent to anyone relevant and, presumably because I have written several pieces on this topic, a copy landed in my Inbox on Wednesday. I interviewed Kahneman about it, and my story about his challenge (my description, not his) is now up at Nature News.
Oxytocin myths are a bit like those big, weighted punching dummies that bounce back up after you take a swing at them. On the flipside, it means that there’s never a shortage of opportunities to talk about the real science behind this massively overhyped hormone. Here’s me on BBC Worldwide last week, chatting about oxytocin research in light of a new study.