By discovering the role of key neurons that mediate an important part of vision development, UC Irvine and UCLA neurobiologists have revealed a new approach to correcting visual disorders in children who suffer from early cataracts or amblyopia, also known as lazy eye.
Such youngsters can have permanent defects in vision, even after surgery to remove cataracts or correct lazy eye. These flaws are often a result of improper brain development due to visual deprivation during childhood. In contrast, when cataracts in adults are surgically corrected, normal vision is usually restored.
Xiangmin Xu, assistant professor of anatomy & neurobiology at UC Irvine, and Josh Trachtenberg, associate professor of neurobiology at UCLA, found that this phenomenon is caused by a specific class of inhibitory neurons that control the time window, or "critical period," in early vision development, generally before age 7. The results of their study appeared online Aug. 25 in Nature.
The researchers discovered that improper functioning of these key neurons during the critical period of development is responsible for these vision defects. Additionally, in tests on mice, they used an experimental drug compound to reopen this critical-period window and treat the neuronal defects associated with temporary loss of vision in one eye during early development.
Their work suggests that drugs targeted to the critical period-regulating neurons can correct central vision disorders in children who've suffered from amblyopia or early cataracts.
"The specific type of neurons that mediate the critical-period window during childhood development have not been well understood until now," Xu said. "Our breakthrough outlines a new path for treatments that can restore normal vision in children who have had early vision disorders."
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