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September 23, 2009 | By:  Jannis Brea
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A New Perspective on Vision

In the early 1960s, Hubel and Wiesel, two of the grandfathers of modern neuroscience, demonstrated that if you block light from one eye in kittens for long enough during their development, the obscured eye will not see as well as the un-obscured eye even after removing the covering.1 

In humans, this condition is known as amblyopia and affects about 2-5% of all people on Earth.2 This time window for change, or neural plasticity, became known as the "critical period" for vision. A lot of work has been done since then to determine exactly when and how this mechanism works, but a preview of an upcoming study challenges this understanding.3

Pawan Sinha, MIT professor and founder of Project Prakash, has worked in India over the past five years treating individuals with curable vision disorders and studying their recovery. 4 Convention holds that most of our visual wiring finishes up by age 5 or 6, but in one case, a 29 year-old man known as S.K. with secondary congenital aphakia, or a lack of lenses, showed remarkable improvement after treatment.

From birth, S.K.'s eyes had been unable to focus on any object, rendering the world a complete blur. As a result, his brain had never learned to distinguish the outline of shapes. When researchers tested his corrected vision, he still had trouble identifying overlapping shapes; his brain instead would break them down into sections. If traditional ideas about vision held true, his ability to distinguish shapes would never improve.

Luckily, this didn't turn out to be the case.

The most interesting part, however, was the role motion played in improving his vision. Once he started looking at moving shapes, his brain quickly learned to recognize them both when moving and still. Furthermore, motion seemed to be the gateway to learning by other characteristics such as color and orientation too. After 18 months, his and other patients' ability to discern still objects almost reached normal levels. 

Before you conclude that these findings seem to contradict the idea of a visual critical period, perhaps take a little deeper look at the animal research. In particular, Harvard neuroscientist Takao Hensch and his team have revealed that the visual critical period can be manipulated.5

By rearing mice in darkness or deleting a specific enzyme known as GAD65, the critical period can be delayed well into adulthood. Once exposed to light or treated with benzodiazepam, the main chemical in the antidepressant Valium, mice reared under these conditions start developing their vision again.

While we don't yet understand what is happening when humans with a variety of vision defects have sight restored, chances are we can still apply the research that we've acquired in one of the oldest fields of neurobiology. It thus pays to be a little skeptical of big black-and-white headlines claiming a big upheaval of this or that theory. More often than not, the truth about the natural world lies in shades of grey.

 

1 T.N. Wiesel and D.H. Hubel. (1963). Single-cell responses in striate cortex of kittens deprived of vision in one eye. J. Neurophysiol. 26: 1003-1017.

J.M. Holmes and M.P. Clarke. (2006). Amblyopia. Lancet 367: 1343-1351.

3 "Cases Of Restored Vision Reveal How The Brain Learns To See." ScienceDaily. September 18, 2009.

4 Here is a link to the Sinha lab website where you can view a list of recent publications and find out more about Project Prakash.

5 Sugiyama S, Di Nardo AA, Aizawa S, Matsuo I, Volovitch M, Prochiantz A, and TK Hensch. (2008) Experience-Dependent Transfer of Otx2 Homeoprotein into the Visual Cortex Activates Postnatal Plasticity. Cell 134 (3): 508-520

 

Image credit: FreeDigitalPhotos.net

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