The human visual system isn’t complete when a baby is born. It develops as a baby sees things. How does that happen? Also, as vision fails due to eye disease, how do the retinal neurons react? Two research projects studied these phenomena and their findings provided more information on how the eye and brain work together.
A study done at The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology (MIT) demonstrated that neurons in the visual cortex are extremely active during postnatal development.
Binocular vision requires many additions and removals of “spine” structures, known as synapses. Scientists tracked hundreds of these structures in mice that house individual network connections on the dendrite branches of visual cortex over 10 days. They found that 40 percent of the synapses that started the process survived.
A graduate student, Katya Tsimring, led the study, which was published in the journal Nature Communications. She was able to image the same dendrites repeatedly over 10 days in the same live mouse during the critical period to determine what happens to synapses over time.
In this study, mice watched black and white gratings with lines of specific orientation that drifted across their field of view. As this is going on, scientists observed both the structure and activity of the neurons’ body and spines along the dendrites. By tracking 793 dendric spines on 14 neurons at days 1, 5 and 10 of the critical period, they could count the addition and loss of spines and the synaptic connections they held. By simultaneously tracking activity at each connection, they could measure how much visual information the neurons received. By relating the structural changes over the critical period, they aimed to uncover how synaptic turnover refines binocular vision.
The amount of change that occurred was surprising. Researchers found that 32 percent of the spines found on day 1 were gone by day 5 and 24 percent that were around on day 5 had been added since day 1. The time between day 5 and 10 showed similar turnover: 27 percent were gone and 24 percent were added. By and large, only 40 percent of the spines seen on day 1 were there at day 10.
As if that weren’t surprising enough, 4 of the 13 neurons they tracked that responded to visual stimuli still responded on day 10. Scientists don’t know why they didn’t respond. They suspect the neurons now served a different function.
Since researchers were tracking activity at the spines, they could see which orientation triggered the activity and how active they were. What they learned over time was that the spines were more likely to last if they were more active and responded to the same orientation that the dendrite preferred. In fact, spines that responded to input from both eyes were more active and more likely to survive than those that responded to just one eye.
Scientists also noticed that over the 10-day span, clusters developed along the dendrites in which neighboring spines were more likely to be active. Throughout the critical period, neurons refined their part in binocular vision by retaining inputs that reinforce orientations preferences, both by the amount of activity and their correlation with their neighbors.
“Both mechanisms are necessary during the critical period to drive the turnover of spines that are misaligned to the soma and to neighboring spine pairs,” the researchers wrote, “which ultimately leads to refinement of [binocular] responses such as orientation matching between the two eyes.”
So, the study at Picower showed that the dendrites in the visual cortex are very busy refining the mechanisms that guide vision during the critical period. What happens when vision starts to fail, as result of retinitis pigmentosa? Do the retinal cells just lay down and die? Work done at the Jules Stein Eye Institute at the University of California Los Angeles (UCLA) and published in the publication Current Biology demonstrated that the retinal cells rewire themselves as vision deteriorates.
In this study, researchers learned that in mouse rod bipolar cells, neurons that normally receive signals from rods that provide night vision are able to form new connections with cones that provide daytime vision when rod cells no longer function. They studied rhodopsin knockout mice that model early retinitis pigmentosa, where rod cells can’t respond to light. The scientists made electrical recordings of rod bipolar cells to observe how these cells acted when the usual inputs were gone. They also used other mouse models that didn’t have specific components of rod signal to learn what triggers the rewiring process. They also did whole-retina electrical measurement.
The researchers found that rod bipolar cells in mice without functional rods showed high-level responses driven by cone cells rather than rod inputs. These responses were strong and had the characteristics of cone-driven signals. The rewiring happened in mice with rod degeneration, but not in mouse models that lacked rod responses without cell death. This implies that the rewiring is caused by the degeneration process, not merely the absence of light or broken synapses. Since little known about how retinal circuits adapt to cell loss, learning about these adaptations could lead to new treatment targets that help preserve vision. These finding demonstrate that the retina can adapt to the loss of rods in order to preserve daytime light sensitivity.
Work at Picower revealed how vision develops. Work at the Jules Stein Eye Institute showed that the retinal cells actively work to preserve daylight vision and that process can be utilized as treatment target. Once again, research shows there is more to vision than meets the eye.
Sources:
https://picower.mit.edu/news/connect-or-reject-extensive-rewiring-builds-binocular-vision-brain
https://www.uclahealth.org/news/release/eye-cells-rewire-themselves-when-vision-begins-fail