A new study has revealed a critical process that allows for correction of visual errors in low light conditions. Perception of light is facilitated by rhodopsin receptors in the eye, which detect small particles of light known as photons. Detection of these photons induces a chemical cascade that eventually translates these signals to the nervous system into the light we see. Previously, it was thought that the strength of the rhodopsin signal was the single factor affecting our ability to see well in dim light, and that more photons detected by rhodopsin led to better visual acuity. However, scientists at UC Davis have shown that there is a second pathway involved. While the rhodopsin receptors are extremely precise, small errors in photon detection by over-active rhodopsin receptors can occur, which can lead to flawed light perception by the brain. This is especially significant in dim conditions, where ‚Äúseeing‚Äù more light than is actually there can be dangerous, such as for a driver at night. The researchers found that hyperactive rhodopsin receptors changed calcium levels at a faster rate than normal rhodopsin receptors. This faster change caused calcium to activate a signal that counteracted the abnormal rhodopsin receptors, hence correcting for the errors and sending accurate information to the nervous system. This discovery may not only lead to new treatments for visual deficits, but it may also help improve normal night vision.