What keeps our retinas from disintegrating each night as glutamate continues to be released is unknown, but growing evidence suggests our molecular protector may be zinc, a metal abundant in tissues throughout the body.

Zinc’s relationship to vision was first recognized when it was found that night blindness is associated with zinc deficiency, and recent studies have shown that a diet supplemented with this trace metal can reduce the progression of one form of age-related blindness. But despite its apparent benefits, not much is known about the relationship between zinc and the eye.

Richard Chappell, a professor of biological sciences at Hunter College, is at the MBL this summer with doctoral student Ivan Anastassov and Harris Ripps, a senior research scientist at MBL and emeritus professor of ophthalmology at the UIC College of Medicine in Chicago, to investigate how zinc may control the wily glutamate. Using the retina of the skate, a cartilaginous fish resembling a manta ray, they record electroretinograms (ERGs) to measure how retinal neurons respond to light stimuli in the presence and absence of normal levels of zinc.

Their preliminary results indicate that ionic zinc (Zn²⁺) is co-released with glutamate from skate rods, and feeds back onto the photoreceptor terminals to suppress the release of glutamate, thus providing an automatic gain control mechanism that reduces the risk of glutamate toxicity.

Demonstrating the role of Zn²⁺ in the regulation of glutamate release from skate rods is still a long way from fully understanding its potential use in therapy for human diseases where glutamate toxicity may be involved, but its ubiquity among vertebrates shows promise. The presence of available Zn²⁺ and/or its transporters has been observed in the photoreceptor region of salamanders, zebrafish, mice, and skates, but “The question is whether this is an integral part of the physiology of the retina,” says Ripps. “Once you understand the normal retina, you can determine the basis of retinal disorders.”

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