Correction of amblyopia in cats and mice after the critical period.

Monocular deprivation early in development causes amblyopia, a severe visual impairment. Prognosis is poor if therapy is initiated after an early critical period. However, clinical observations have shown that recovery from amblyopia can occur later in life when the non-deprived (fellow) eye is removed. The traditional interpretation of this finding is that vision is improved simply by the elimination of interocular suppression in primary visual cortex, revealing responses to previously subthreshold input. However, an alternative explanation is that silencing activity in the fellow eye establishes conditions in visual cortex that enable the weak connections from the amblyopic eye to gain strength, in which case the recovery would persist even if vision is restored in the fellow eye. Consistent with this idea, we show here in cats and mice that temporary inactivation of the fellow eye is sufficient to promote a full and enduring recovery from amblyopia at ages when conventional treatments fail. Thus, connections serving the amblyopic eye are capable of substantial plasticity beyond the critical period, and this potential is unleashed by reversibly silencing the fellow eye.

Naturally occurring strabismus in monkeys (Macaca nemestrina).

Seven naturally strabismic monkeys (Macaca nemestrina) was identified. Five of these monkeys were examined by ophthalmologists. No ophthalmoscopically obvious cause for the squint was found in any case. Of those five animals, two were tested behaviorally on visual responsiveness and visual acuity. The acuity of both eyes of both monkeys was somewhat poorer than normal. In addition, an amblyopia of 0.8 octaves was found for one monkey and 0.6 octaves for the others. The existence of naturally strabismic monkeys supports the utility of the macaque as an animal model for studying strabismus and amblyopia.