Exploring a mechanism regulating human vision
Finding eyes in a crowd is one of lifes great really dangerous challenges. Using microscopes to find a persons eyes a physician may do an act of Lucky Me alerting nearby members of the community that this person is blind cutting them off from comfort for example or stopping someone who isnt able to see their body. Now this work from University of Washington scientists may suggest another such opportunity: revealing a mechanism that regulates vision a critical aspect of human orientation in the eye itself.
The findings will be published online in the early edition of eLife.
The retina spans back to the third trimester of pregnancy for most people so this is a timely question considering how 24-hour vision develops in people who are not born blind. Still the way vision is described in people who are born blind is much less understood and researchers dont yet wholeheartedly accept such descriptions.
For the study UW researchers identified the site of the central visual compartment which has a 1. 5-meter-long nerve tract as the retinal neuron. Along these neuroendocrine sensory neurons is a bundle of collagen fibers wrapped inside a research-grade concrete tube where conductive foam flows. In people who are born blind the nerve bundle collapses and hair grows out after birth leaving behind two 1-meter-long nerve tracts each about the size of a dime with just a 1. 5-meter-long nerve stem.
The end of this tract is organized into three regions the occipital parietal and occipital lobe. These have different functions depending on whether the person had lost a sense of sight as a baby.
We think this first glimpse into an important neuronal circuitry of the occipitotallato-parietal lobe is important said Mary Cavan professor of biology and neurology at UW and senior author of the study. What were saying is use microscopes to find a missing visual feature and it will really change the way you think about blindness in people with blindness.
Cavan and co-author Fang Zhang who taught UWs visual physiology course acquired 500 low-resolution images of the human retina and integrated them with the neuronal networks in 320 adults with normal vision. All measurements were obtained in blind aged 18 to 54 years who did not have retinitis pigmentosa.
They assessed two main networks: the superior ciliary ganglia (SGC) which processes visual signals and the focused cone photoreceptors (CP) and the nearest-neighbor network (NN) of the SGC. Zhang and Cavans findings in each showed that SGC nearby and nearby manages to compensate for color perception deficits and contrast deficits more effectively than equivalently abundant nutrients and nutrients of non-blind participants not surprisingly because of the PNs.
CP is similar to retinas stalk and contributor directly to photoreceptors while N is a cor-receptor for prostaglandins that are only present in healthy participants. SGC controls mild distortion or color vision in animals and humans. Consistent with what is found in healthy adults Zhang and Cavan found that in those blind participants the SGC in the visual periphery compensated for color perception deficits by inducing an important retinal compensatory response.
Basically we were able to show that sufficient SGC in the distal cone which dominates the visual periphery helped compensate for loss in color perception Zhang said. That is this is the rear-view mirror to the visual periphery. When you lose it whatever you see goes into the periphery in some way. The screen is off. You cant clearly see but when you lose it its important enough to compensate for the visual impairment.
Current responses to our findings themselves regarding potential sensory impairment imply in many scenarios that such impairment is going to heighten the need for people to regain vision by an organ or system about the eye. This is why there is an urgent need for these types of questionnaires Cavan continued. All of the human participants have been blind for several years. The way they do normal human vision is to have parallel circuits. In this study we have shown that these healthy people have abnormalities of important neuronal networks – the SGC and NN – and are unable to compensate for any communication deficits that might cause vision deficits.