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Eye cells 'rewire' their connections when vision loss begins, scientists find
Last reviewed: 15.07.2025
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Scientists at the Jules Stein Eye Institute at the David Geffen School of Medicine at UCLA have discovered that certain retinal cells can reprogram themselves when vision begins to deteriorate in retinitis pigmentosa, an inherited eye disease that leads to progressive blindness.
In a study of mice, the researchers found that rod bipolar cells — neurons that typically receive input from rods, which mediate night vision — can form new functional connections with cones, which mediate daytime vision, when their usual partners stop working. The findings are published in the journal Current Biology.
Retinitis pigmentosa affects millions of people worldwide and is one of the leading causes of inherited blindness. Although the disease often progresses slowly and some patients retain significant vision into middle age, little is known about how the retina adapts to cell loss. Understanding these natural adaptations may help identify new targets for vision-preserving therapies.
The scientists used mice with a knockout gene for rhodopsin, which models the early stage of retinitis pigmentosa, when rods cannot respond to light and degeneration occurs slowly. They made electrical measurements on individual rod bipolar cells to see how these cells behave when their normal signals are lost.
The team also used other mouse models lacking various components of the rod signaling system to figure out what triggers the rewiring process. Their results at the single-cell level were confirmed by measurements of electrical activity across the entire retina.
In mice with rod degeneration, rod bipolar cells showed strong responses driven by signals from cones rather than their usual sources. These new connections showed the characteristic electrical signature of cone signals.
The rewiring only occurred in mice with rod degeneration and was not observed in other models where rods were unresponsive to light but the cells themselves did not die. This suggests that the rewiring of neural connections is triggered by the degeneration process itself, and not simply by the absence of light signals or the destruction of synapses.
These findings complement a 2023 study by the same group that showed that individual cones can remain functional even after severe structural changes in the late stages of the disease. Together, these studies demonstrate that the retina uses different adaptation mechanisms at different stages of disease progression.
"Our results show that the retina adapts to the loss of rods in a way that tries to preserve sensitivity to daylight," said lead author A.P. Sampat, PhD, of the Jules Stein Institute.
"When the normal connections between rod bipolar cells and rods are lost, these cells are able to rewire themselves to receive signals from cones. It appears that the signal for this plasticity is the degeneration itself, perhaps through the role of glial support cells or factors released by dying cells."
One open question is whether this rewiring is a general mechanism used by the retina when rods die. The team is now investigating this process in other mutant mice with defects in rhodopsin and other rod proteins that are known to cause retinitis pigmentosa in humans.