This work has the long-term goal of understanding myopia in the context of the biological processes by which the growth of the eye is controlled. It seems reasonable to view myopia not as a disease state, but as a defect in the process by which the eye grows toward being emmetropic (that is, neither myopic nor hyperopic). The proposal seeks to determine at what levels the control over the growth of the young eye is exerted. Specifically, we find that there is a retinal level of control, manifested by visual deprivation of a part of the retina causing the growth of the sclera only in the deprived region, apparently without the participation of the brain. We propose to study this by raising birds with one region of the retina deprived of form vision and comparing the refractive status and size of the deprived region with the visually experienced region. Then we will do the same in animals with the optic nerve severed. Preliminary indications are that visual deprivation can still produce a local myopic region even under these conditions. If simple form deprivation causes severe myopia, it may be the case that the simple chaotic visual stimulation of a strobe light can prevent myopia from developing. We propose to test this in several species. We suspect that it is not the case that all control of the growth of the eye comes from within; we plan to assess the role of the brain in experimental myopia by making lesions in the Edinger-Westphal nucleus as well as by cutting the optic nerve. We also plan to study the process by which some eyes, such as those of chicks, can recover from myopia, whereas others cannot. We wish to explore the possibility that the same internal factors that determine an individual's susceptibility to myopia also determine its ability to recover from the myopia.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY002727-11
Application #
3257109
Study Section
Visual Sciences B Study Section (VISB)
Project Start
1978-12-01
Project End
1992-03-31
Budget Start
1989-04-01
Budget End
1990-03-31
Support Year
11
Fiscal Year
1989
Total Cost
Indirect Cost
Name
City College of New York
Department
Type
Schools of Arts and Sciences
DUNS #
603503991
City
New York
State
NY
Country
United States
Zip Code
10031
Zhu, Xiaoying; McBrien, Neville A; Smith 3rd, Earl L et al. (2013) Eyes in various species can shorten to compensate for myopic defocus. Invest Ophthalmol Vis Sci 54:2634-44
Zhu, Xiaoying (2013) Temporal integration of visual signals in lens compensation (a review). Exp Eye Res 114:69-76
Sheng, Caren; Zhu, Xiaoying; Wallman, Josh (2013) In vitro effects of insulin and RPE on choroidal and scleral components of eye growth in chicks. Exp Eye Res 116:439-48
Nickla, Debora L; Zhu, Xiaoying; Wallman, Josh (2013) Effects of muscarinic agents on chick choroids in intact eyes and eyecups: evidence for a muscarinic mechanism in choroidal thinning. Ophthalmic Physiol Opt 33:245-56
Rucker, Frances J; Wallman, Josh (2012) Chicks use changes in luminance and chromatic contrast as indicators of the sign of defocus. J Vis 12:
Leung, Tsz-wing; Flitcroft, Daniel I; Wallman, Josh et al. (2011) A novel instrument for logging nearwork distance. Ophthalmic Physiol Opt 31:137-44
Nickla, Debora L; Wallman, Josh (2010) The multifunctional choroid. Prog Retin Eye Res 29:144-68
Zhu, Xiaoying; Wallman, Josh (2009) Temporal properties of compensation for positive and negative spectacle lenses in chicks. Invest Ophthalmol Vis Sci 50:37-46
Zhu, Xiaoying; Wallman, Josh (2009) Opposite effects of glucagon and insulin on compensation for spectacle lenses in chicks. Invest Ophthalmol Vis Sci 50:24-36
Rucker, Frances J; Wallman, Josh (2009) Chick eyes compensate for chromatic simulations of hyperopic and myopic defocus: evidence that the eye uses longitudinal chromatic aberration to guide eye-growth. Vision Res 49:1775-83

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