There was no way the blind mice could see, yet somehow, they could. The year was 1923, and a Harvard grad student named Clyde Keeler had set out to compare eyes from different animals, starting with mice that he bred in his dorm room. Keeler cut open one mouse’s eye and put it under a microscope. Immediately he realized something was wrong. Missing from the eye was the layer of rods and cones, the photoreceptors that catch light. Turning back to his colony, Keeler realized that half of his animals were blind. Somehow a mutation had arisen, wiping out their rods and cones.
The mutation had blinded those mice with surgical precision, yet for reasons lost to history, Keeler got the strange idea to shine a light in their eyes anyway. Based on everything that scientists knew about mammalian eyes, nothing should have happened. After all, the mice had no way to capture light and relay it to the retinal ganglion cells, the neurons that normally pass visual signals on to the brain. And yet something did happen: The mouse pupils shrank.
Keeler struggled to find an explanation. “We may suppose that a rodless mouse will not see in the ordinary sense,” he wrote in one journal article. But for pupils to shrink, such mice had to have some kind of cell besides rods and cones—one that scientists knew nothing about—that could also capture light and send a signal to the brain.
