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Unit 4: Lesson 1

Foundations of behavior passages

Could complete darkness be the cure for amblyopia?


Amblyopia, or lazy eye, is a common condition of visual impairment caused by unbalanced neural transmission. The lazy eye itself functions normally, but the optical neurons connected to that eye fail to transmit visual information to the brain. Treatment for amblyopia consists of placing a patch over the healthy eye to prevent light from entering, a procedure known as monocular deprivation (MD). The darkness causes photopigments retinal and opsin to combine into rhodopsin. More importantly, the amblyopia is cured through induced neural modification. In other words, MD causes the brain to re-route most of the nerve connections with the good eye to the lazy one, improving the vision of the lazy eye. Both eyes contribute visual input to each cerebral hemisphere, facilitating this process. MD must be done in early development, when neurons have higher plasticity, or the ability to form new connections. With aging, neuroplasticity is brought to a halt, resulting in permanent vision loss of the lazy eye for amblyopia patients.
Plasticity in kittens is reduced to almost zero at postnatal day 90 (P90), and, past this point, amblyopia treatment is ineffective. Scientists performed two experiments to test the effects of darkness on amblyopia.
Experiment 1: Kittens with normal vision that undergo MD become amblyopic. Scientists induced amblyopia in kittens by suturing one eye shut for 7 days (P30 to P37). At P38, the kittens were amblyopic, and their visual acuity was then continuously measured for 3 months (Figure 1). At P93, scientists placed these kittens in total darkness for 10 days. Afterward, they continued to measure the visual acuity of both eyes (Figure 1).
Experiment 2: One of the mechanisms through which darkness leads to amblyopia recovery involves specifically decreasing levels of molecules that constrain neuronal plasticity, such as the neurofilament protein NF-L. Up to P40, NF-L proteins are low, but gradually rise to 60% of adult values by P90. To verify the effect of dark rearing on plasticity, scientists measured NF-L levels on animals that were raised with normal vision until P30, at which point they were reared in darkness for either 5, 10, or 15 days. (Figure 2).
Figure 1. Amblyopia was induced by a 7 day monocular lid suture in kittens aged 30 days. After re-opening the eye at P37, visual acuity (y axis) was assessed daily for the non-deprived eye (dotted curve) and deprived eye (solid line). After 90 days, kittens were placed again in a completely dark room for a period of 10 days, after which their visual acuity was measured again. A visual acuity score of 6.7 is considered normal vision.
Figure 2. The effects of dark rearing (DR) on NF-L levels of normal-vision kittens placed in a dark room for 5, 10, or 15 days after P40. Treatments 10 day DR and 15 day DR are significantly different from P40 normal.
Adapted from: Kevin R. Duffy, Donald E. Mitchell. 2013. Darkness alters maturation of visual cortex and promotes fast recovery from monocular deprivation. Current Biology, 23, pp. 382–386
What could be expected of the photopigment levels in P110 to P120 of Experiment 1?
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