Shedding light on premature vision

Premature vision causes an aberrant development of neuronal circuits in the primary visual cortex of ferrets.

Newborn squirrel with closed eyes. Image credit: Senthil Kumaran (CC0)

The developing brain requires the right experiences at the right time to form proper connections. For most mammals, vision develops in two main stages. Before birth in humans – or before eye opening in animals born with closed eyes – spontaneous activity within the brain helps establish an initial visual circuitry without external visual input. These initial connections are then fine-tuned after birth or eye opening.

This sequential development is critical for normal visual function. Moreover, the visual system processes different aspects of vision (like motion, direction and detail) through specialized neural pathways, and proper development of these pathways also requires the right sequence of experiences.

In humans, babies born prematurely receive visual stimulation during what would typically be a pre-visual period, potentially disrupting this sequence. To find out what happens when visual experience occurs too early Griswold and Van Hooser studied the developing visual system in ferrets by artificially opening one or both eyes before they would naturally open and recording how neurons of the visual system responded to moving stimuli.

The results showed that ferrets with prematurely opened eyes developed significant abnormalities in their visual processing, particularly in how neurons respond to moving stimuli. Using electrophysiological recordings in the primary visual cortex, Griswold and Van Hooser observed that neurons in the ferrets showed unusually broad responses to different speeds of motion and increased activity at slow speeds. These neurons also showed higher spontaneous activity levels and increased suppression of activity in response to certain stimuli, such as quickly moving grating stimuli. These changes in firing rates and suppression occurred even in a part of the visual cortex that was ipsilateral (on the same side) to the early-opened eye, a location that does not receive direct input from the early-opened eye, suggesting that premature vision causes widespread alterations in brain circuit development. Other aspects of vision, like the ability to detect detail, were less affected.

These findings suggest that the timing of visual experiences is critical for healthy development and may help explain why human infants born very prematurely often have difficulty with motion perception, even without brain injuries. Understanding these neural differences could guide the development of targeted visual therapies for premature infants. Further research could determine if specific types of visual stimulation (or a lack of stimulation) might be protective during this sensitive period.