In a nutshell: Even if the primary visual cortex is damaged — causing blindness — the pathway that transmits visual information from the retina is not completely destroyed. The penultimate stop on the pathway still processes visual information, even if it has nowhere to go.

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In humans and other primates, visual information is transmitted from the retina to a part of the brain called the lateral geniculate nucleus (LGN), before reaching the primary visual cortex (V1). If the V1 is damaged, conscious vision is lost in the area of the visual field that corresponds to the damage. However, some individuals with V1 damage can respond to visual stimuli in the area of blindness without being aware that they can see it. This phenomenon, known as ‘blindsight’, has important implications for our understanding of how the brain works, develops, and adapts to damage.

V1 lesions cause severe cell death in the LGN – as if these cells give up when their transmissions aren’t received. However, recent studies have suggested the LGN is still important for blindsight. Brain Function CoE researchers Hsin-Hao Yu, Nafiseh Atapour and Marcello Rosa, along with their colleagues at Monash University, wanted to reconcile these seemingly contradictory findings by investigating what kind of visual information is carried by the surviving brain cells in the LGN after damage to V1.

The team measured the response properties of LGN cells in marmosets, long after the animals had recovered from a V1 lesion that happened at a distinct developmental stage: just after birth, in early adulthood, or in late life. According to what had been thought for over a century, the LGN cells should have already degenerated by this stage.

The researchers found that, although the V1 lesions caused the size of the LGN to decrease significantly, the surviving LGN cells (about one-third of the original number) retained a remarkable level of visual function – regardless of when the lesion occurred. Most surprisingly, the LGN cells still responded to visual information that came from inside the area of blindness.

The group’s results confirm the hypothesis that the LGN could support blindsight. Their findings also suggest that this cell population could be a promising target for future treatments to restore partial vision following stroke.

Next steps:
The team will investigate which areas of the brain receive the information sent by the surviving LGN cells, to further understand how this information can be used.

Yu, H.-H., Atapour, N., Chaplin, T. A., Worthy, K. H., & Rosa, M. G. P. (2018). Robust visual responses and normal retinotopy in primate lateral geniculate nucleus following long-term lesions of striate cortex. Journal of Neuroscience, doi: 10.1523/JNEUROSCI.0188-18.2018

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