One of the most irritating reflexes to us as humans is the glaring light that awakens us after a hard night of studying, or causes our eyes to water after a doctor shines a penlight in them. It has become a well-known fact among the pre-medical community here at Hopkins (and even most of the general population that avidly watches Grey's Anatomy) that when a doctor shines a light in the eyes of an unconscious patient to assess reflexes, it gives some insight into brain activity, as it controls constriction of the pupil. Yet researchers at Hopkins have shed light — no pun intended — on whether the brain does, in fact, control this reflex.
Amphibians and fish have long been known to have photosensitive irises, which do not necessitate brain function in order for their eyes to react to light. Yet mammals, such as ourselves, have been suspected of needing our gray matter for this reflex, until the team, led by King-Wai Yau, a professor of Neuroscience and Ophthalmology at the Hopkins School of Medicine, found that melanopsin, a specialized pigment that is located in the retina's ganglion cells, are responsible for the pupillary light reflex.
Researchers at the Hopkins School of Medicine collaborated with Harvard Medical School, Children's Hospital Boston, California Institute of Technology and the Universitat des Saariandes in Germany in their experiment. They used irises that had been isolated from mammals and attached a meter to determine the force of the muscle that controls the pupil (the sphincter muscle) when light was shined on the pupil. The majority of nocturnal animals, with the exception of the owl monkey and bush baby, showed a response to light, while most diurnal animals did not. The researchers believe that animals that have begun to follow the sleep-wake cycle of humans lack the ability to see at night (much like we cannot see in the dark), and propose that nocturnal animals have more cells in the eye that are sensitive to lower amounts of light exposure. Bright light might cause damage, and the pupil's reflex may have been an adaptation to protect against vision loss.
Yau suspected that melanopsin was involved in this mechanism, as he had worked with mice in the past that he had genetically engineered to lack the protein. The researchers tested irises isolated from the mice to see if they would respond, and found that they lacked the pupillary light reflex. Mice that had been genetically engineered to lack other pigments known to capture light all retained the reflex.
Protein Lipace C, an enzyme that interacts with melanopsin, is known to be responsible for the same pathway in the vision system of flies. The team then tested this in mice that lacked the enzyme, and found that they also lacked the response, making it a prime suspect along with melanopsin that is responsible for the reflex.
Although the local reflex in the eye itself has been identified, the team still has questions relating to which proteins in the muscles cause the contraction.
