Soon, we’ll be reading your minds!

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No, not really, but this is still a cool result: investigators have used an MRI to read images off the visual cortex. They presented subjects with some simple symbols and letters, scanned their brains, and read off the image from the data — and it was even legible! Here are some examples of, first, the images presented to the subjects, then a set of individual patterns from the cortex read in single measurements, and then, finally, the average of the single scans. I think you can all read the word “neuron” in there.

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Reconstructed visual images. The reconstruction results of all trials for two subjects are shown with the presented images from the figure image session. The
reconstructed images are sorted in ascending order of the mean square error. For the purpose of illustration, each patch is depicted by a homogeneous square,
whose intensity represents the contrast of the checkerboard pattern. Each reconstructed image was produced from the data of a single trial, and no postprocessing was applied. The mean images of the reconstructed images are presented at the bottom row. The same images of the alphabet letter ”n” are displayed in
the rightmost and leftmost columns.

Before you get all panicky and worry that now the CIA will be able to extract all of those sexy librarian fantasies out of your brain by aiming a gadet at your head, relax. This is an interesting piece of work, but it has some serious limitations.

  • This only works because they are scanning the part of the visual cortex that exhibits retinotopy — a direct mapping of the spatial arrangement of the retina (and thus, of any images falling on it) onto a patch of the brain at the back of your head. This won’t work for just about any other modality, except probably touch, and I doubt it will work for visualization/cognition/memory, which are all much more derived and much more complexly stored. Although I’d really like to know if someone closes their eyes and merely imagines a letter “E”, for instance, whether there isn’t some activation of the visual cortex.

  • The process was time consuming. Subjects were first recorded while staring at random noise for 6 seconds in 22 trials. This was necessary to get an image of the background noise of the brain, wwhich was subtracted from subsequent image measurements. The brain is a noisy place, and the letter pattern is superimposed on a lot of background variation. Then, finally, the subject has to fixate on the test image for 12 seconds.

  • Lastly, a fair amount of math has to be flung at the scan to extract the contrast information. This is probably the least of the obstacles, since computational power seems to increase fairly rapidly.

Give this research some more time, though, and I can imagine some uses for being able to record specific aspects of brain states. I’d be more interested in a device that can read pre-motor cortex though — I’d like to get rid of this clumsy keyboard someday.

Miyawaki Y, Uchida H, Yamashita O, Sato M-a, Morito Y, Tanabe HC, Sadato N, Kamitani Y (2008) Visual Image Reconstruction from Human Brain Activity using a Combination of Multiscale Local Image Decoder. Neuron 60(5):915-929.

A Natural History of Seeing: The Art and Science of Vision

Simon Ings has written a wonderful survey of the eye, called A Natural History of Seeing: The Art and Science of Vision(amzn/b&n/abe/pwll), and it’s another of those books you ought to be sticking on your Christmas lists right now. The title give you an idea of its content. It’s a “natural history”, so don’t expect some dry exposition on deep details, but instead look forward to a light and readable exploration of the many facets of vision.

There is a discussion of the evolution of eyes, of course, but the topics are wide-ranging — Ings covers optics, chemistry, physiology, optical illusions, decapitated heads, Edgar Rice Burroughs’ many-legged, compound-eyed apts, pointillisme, cephalopods (how could he not?), scurvy, phacopids, Purkinje shifts…you get the idea. It’s a hodge-podge, a little bit of everything, a fascinating cabinet of curiousities where every door opened reveals some peculiar variant of an eye.

Don’t think it’s lacking in science, though, or is entirely superficial. This is a book that asks the good questions: how do we know what we know? Each topic is addressed by digging deep to see how scientists came to their conclusion, and often that means we get an entertaining story from history or philosophy or the lab. Explaining the evolution of our theories of vision, for example, leads to the story of Abu’Ali al-Hasan ibn al-Hasan ibn al-Haythem, who pretended to be mad to avoid the cruelty of a despotic Caliph, and who spent 12 years in a darkened house doing experiments in optics (perhaps calling him “mad” really wasn’t much of a stretch), and emerged at the death of the tyrant with an understanding of refraction and a good theory of optics that involved light, instead of mysterious vision rays emerging from an eye. Ings is also a novelist, and it shows — these are stories that inform and lead to a deeper understanding.

If the book has any shortcoming, though, it is that some subjects are barely touched upon. Signal transduction and molecular evolution are given short shrift, for example, but then, if every sub-discipline were given the depth given to basic optics, this book would be unmanageably immense. Enjoy it for what it is: a literate exploration of the major questions people have asked about eyes and vision for the last few thousand years.

Usher syndrome part IV: Clinical management and research directions

Guest Blogger Danio, one last time:

Part I
Part II
Part III

The current standard of pediatric care mandating that all newborns undergo hearing screenings has been applied successfully throughout much of the industrialized world. Early identification of hearing impairments gives valuable lead-time to parents and health care providers during which they can plan medical and educational interventions to improve the child’s development, acquisition of language skills, and general quality of life.

Up to 12% of children born with hearing loss have Usher syndrome. However, diagnosing Usher syndrome as distinct from various forms of congenital hearing impairment is often impossible until the onset of retinal degeneration years later. The considerable number and size of the genes involved makes genetic screening impractical with the current methods, unless there is a family or community history that can shorten the list of targets by implicating a particular Usher gene or subtype.

The educational and medical interventions undertaken to improve a deaf or hearing-impaired child’s cognitive and social development can vary extensively, based in part on whether the child in question is expected to lose his or her vision later in life. Thus an earlier diagnosis of Usher syndrome is an immediate and critical research goal. The most imminent hope for such a diagnostic advance lies in gene chip screening. With this technology, the patient’s DNA can be screened against a microarray of human genes known to cause deafness (and/or Usher syndrome) when mutated, and variances in the DNA sequence of any screened gene would be detected and analyzed. One such chip is already available for commercial use, and another appears to be approaching clinical availability. The rapid and affordable analysis these microarrays offer will be of tremendous benefit in the early diagnosis and management of Usher syndrome.
[Read more…]

Usher syndrome, part III: the plot thickens

Guest Blogger Danio:

The time has come to delve into the retinal component of Usher syndrome. In Part II, I briefly described the results of protein localization studies, in which most members of the Usher cohort were found at the connecting cilium of the photoreceptor and at the photoreceptor synapse. The following diagram summarizes these findings:

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Usher protein localization in photoreceptor cells. From Reiners, et al. 2006

So, as we saw in the ear, proteins with the equipment for physically interacting with one another are gathering in specific places, and thus multi-protein complexes are likely being formed at these locations. The cluster of Usher proteins around the connecting cilium has been the focus of most of the current retinal studies, and to understand the potential importance of an Usher complex at that subcellular location we must address the importance of the connecting cilium itself.
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Usher syndrome, Part II: A complex molecular picture

Guest Blogger Danio:

I know, I know. Friday night isn’t exactly the best time to smack you with a big messy fistful of science, but PZ will be kicking us Minions out of the house early next week, so I have to stay on schedule with these Usher posts if I’m going to get through Part IV by the time he shows me the door.

In Part I, I introduced the hereditary disease known as Usher syndrome and went over a bit of the cell biology of auditory and visual sensory cells. In this post, I’ll discuss the molecules known to be affected in Usher patients, and begin to describe what is known about their function.

As mentioned previously, variations in the clinical presentation of Usher syndrome have resulted in the creation of three clinical subtypes. Type 1 is characterized by severe to profound congenital hearing loss, balance problems, and early onset vision loss, usually beginning before the patient’s 10th birthday. The type 2 hearing loss is also congenital, but tends to be less severe. The vision loss in type 2 usually begins to occur a bit later, in the early teen years, and these patients do not present with balance problems. All three categories of symptoms–vision, hearing, and balance, are progressive, commencing in childhood or adolescence rather than at birth, in Usher type 3 patients.

Despite these differences, the specific combination of deaf-blindness, plus or minus balance defects, led researchers to predict that multiple mutations in a single gene, or perhaps in two or three genes at the most, would turn out to be responsible for the symptoms observed in all Usher patients. The advent of genetic mapping led to surprising results in this regard. To date, at least 11 different genes have been implicated in the disease, nine of which have been molecularly identified thus far. More surprising still are the natures of the proteins encoded by the identified genes. In contrast to signaling or metabolic pathways, in which a genetic defect at any point in the regulatory chain of events will adversely affect the target and result in an abnormal phenotype, the Usher proteins do not act in stepwise fashion to regulate a cellular process. What they actually do is not entirely clear at this point, but the various proteins contain functional domains known to be important for scaffolding, cell adhesion and signaling, extracellular matrix formation, and motor activity.
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Usher syndrome, Part I: an introduction to sensory perception

Guest Blogger Danio:

In my introductory post I mentioned that my research focuses on the genetics of hereditary deaf-blindness, specifically Usher syndrome. As it’s likely that many of you have never heard of it, I thought I’d kick it up a notch with some sciency posts on what we know about Usher syndrome and what we think we can contribute to the diagnosis and treatment of the disease.

Usher syndrome is a genetically recessive condition characterized by hearing impairment, usually from birth, which is due to the degeneration of sensory neurons in the inner ear, and blindness due to retinal degeneration, which begins to occur in childhood or adolescence and progresses through several decades. Additionally, some Usher patients have balance problems associated with the sensory cell loss in the ear. There is a great deal of variation in the clinical presentation of the disease, and three clinical subtypes can be classified by the severity and age of onset of the symptoms. Usher syndrome affects about 1 in 17,000 Americans, and there are a number of populations around the world where the incidence is higher due to founder effects or intermarriage.

To begin to understand the pathology of this disease, one needs to focus on the affected cell types: mechanosensory hair cells and photoreceptors. Both are highly specialized types of sensory cells, but they’re performing essentially the same function, namely receiving an environmental stimulus and converting it into an electrical signal that is transmitted to the brain for interpretation. Although the nature of the stimuli–sound and light–are quite different, they are processed in much the same way, and thus it is not surprising to find a number of structural and functional similarities between photoreceptors and hair cells.
[Read more…]

It’s got a good beat and you can dance to it

My first of several posts about sensory cell neurobiology will be appearing shortly. To get you warmed up, here’s a movie showing a mechanosensory hair cell responding to a low frequency sound played through the glass pipette you can see in the image. *Caution*: low frequency sound may not be appropriate for work. Earphones recommended.

Also, the Scienceblogs Survey is now open again, and will remain so until 11PM EST Friday, August 15th.

~Danio

Evolving proteins in snakes

Blogging on Peer-Reviewed Research

We’ve heard the arguments about the relative importance of mutations in cis regulatory regions vs. coding sequences in evolution before — it’s the idea that major transitions in evolution were accomplished more by changes in the timing and pattern of gene expression than by significant changes in the genes themselves. We developmental biologists tend to side with the cis-sies, because timing and pattern are what we’re most interested in. But I have to admit that there are plenty of accounts of functional adaptation in populations that are well-founded in molecular evidence, and the cis regulatory element story is weaker in the practical sense that counts most in science (In large part, I think that’s an artifact of the tools — we have better techniques for examining expressed sequences, while regulatory elements are hidden away in unexpressed regions of the genome. Give it time, the cis proponents will catch up!)

This morning, I was sent a nice paper that describes a pattern of functional change in an important molecule — there is absolutely no development in it. It’s a classic example of an evolutionary arms race, though, so it’s good that I mention this important and dominant side of the discipline of evolutionary biology — I know I leave the impression that all the cool stuff is in evo-devo, but there’s even more exciting biology outside the scope of my tunnel vision. Also, this paper describes a situation and animals with which I am very familiar, and wondered about years ago.

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How do you make a cephalopod drool?

Blogging on Peer-Reviewed Research

We’re all familiar with Pavlov’s conditioning experiments with dogs. Dogs were treated to an unconditioned stimulus — something to which they would normally respond with a specific behavior, in this case, meat juice which would cause them to drool. Then they were simultaneously exposed to the unconditioned stimulus and a new stimulus, the conditioned stimulus, that they would learn to associate with the tasty, drool-worthy stimulus — a bell. Afterwards, ringing a bell alone would cause the dogs to make the drooling response. The ability to make such an association is a measure of the learning ability of the animal.

Now…how do we carry out such an experiment on a cephalopod? And can it be done on a cephalopod with a reputation (perhaps undeserved, as we shall see) as a more primitive, less intelligent member of the clade?

The nautilus, Nautilus pompilius despite being a beautiful animal in its own right, is generally regarded as the simplest of the cephalopods, with a small brain lacking the more specialized areas associated with learning and memory. It’s a relatively slow moving beast, drifting up and down through the water column to forage for food. It has primitive eyes, which to visual animals like ourselves seems to be a mark of less sophisticated sensory processing, but it has an elaborate array of tentacles and rhinophores which it uses to probe for food by touch and smell/taste. Compared to big-eyed, swift squid, a nautilus just seems a little sluggish and slow.

So let’s look and see how good a nautilus’s memory might be. First, we need a response to stimuli that we can recognize and measure, equivalent to the drooling of Pavlov’s dogs. While they don’t measurably salivate, the nautilus does have a reaction to the hint of something tasty in the water — it will extend its tentacles and rhinophores, as seen below, in a quantifiable metric called the tentacle extension response, or TER.

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The scoring system for tentacle extension response (TER) in chambered nautilus. TER was graded every 5 s from a minimum score of 0 to a
maximum score of 3. Each level corresponds to a range of percentage extension relative to the length of the animalʼs hood. Zero is recorded when all
tentacles are retracted into their sheaths. A score of 1 corresponds to an extension of <33% of the hood length. A score of 2 corresponds to extension
between 34% and 66%, and 3 is given when tentacles are extended beyond 67% of hood length.

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