Blindsight’s origins uncovered

No, not the (excellent) Peter Watts novel… but the neurological phenomenon for which it is named. Ars Technica boils down a new paper published in Nature:

The authors worked with two macaques that have small lesions in their primary visual cortexes, which leave them unable to respond to visual cues in a subset of their visual field. A fair amount of work went in to defining precisely the areas within the visual field that were no longer effective, and confirming that stimuli in those areas could still induce activity (measured via functional MRI) in the remaining visual cortexes.

The authors then focused on a structure called the lateral geniculate nucleus (LGN), which acts as a relay point for signals travelling between the retina and the primary visual cortex. Other work had shown that the LGN also has projections to a number of secondary visual areas, suggesting that it may serve as a major hub in the visual system.

To test this suggestion, the authors injected the LGN with a chemical that activates the receptor for a major inhibitory signaling molecule (the chemical, THIP, is what’s termed a “GABAA-receptor agonist”). When the chemical is present, nerve cells receive a signal telling them to stop signaling, so this this injection has the effect of shutting the LGN down entirely.

The treatment was highly effective. With the LGN shut down, visual stimuli that normally induce a blindsight response didn’t elicit any response from the visual centers of the macaques.

And here’s a blindness-related bonus story with some feel-good we-can-fix-anything-eventually overtones (as well as some science-not-the-work-of-Beelzebub-after-all undertones) to set you up for the weekend: restoring sight to blinded human patients with stem cell therapy. Yay, science!

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