April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Mammalian Eyes Need an Intact Optic Nerve to Detect the Sign of Defocus During Emmetropisation
Author Affiliations & Notes
  • S. A. McFadden
    School of Psychology, University of Newcastle, Callaghan, Australia
  • C. Wildsoet
    School of Optometry, University of California, Berkeley, California
  • Footnotes
    Commercial Relationships  S.A. McFadden, None; C. Wildsoet, None.
  • Footnotes
    Support  International Science Linkages GO120160, NIH R01EY012392-09
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1620. doi:
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      S. A. McFadden, C. Wildsoet; Mammalian Eyes Need an Intact Optic Nerve to Detect the Sign of Defocus During Emmetropisation. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1620.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Myopia is caused by aberrant visual input to the eye during development. Form deprivation causes myopia in mammals, even when the eye is disconnected from the brain with TTX1. Mammalian eyes partially form deprived, elongate only in the corresponding sector implying local retinal control of myopia2. Eyes also modify growth when wearing minus or plus spectacle lenses, becoming myopic from accelerated growth or hyperopic from inhibited growth, respectively. We asked whether mammalian eyes compensate for spectacle induced defocus when disconnected from the brain after optic nerve section (ONS).

Methods: : Guinea pigs underwent either ONS or Sham surgery at ~4 days of age. A +4D (n=16) or -4D (n=13) spectacle lens was worn on one eye for 2 weeks from 8-22 days of age. Corneal power, refractive error and ocular parameters were measured before surgery, before, during and after lens wear, and after lens removal. To assess the effects of ONS alone, 9 animals underwent ONS but did not wear lenses.

Results: : Sham eyes responded like normal eyes 3 to defocusing lenses (-4D: -5.2D; +4D: +0.4D after 2 weeks of lens wear). However, ONS eyes wearing lenses developed excessive myopia, regardless of the sign of imposed defocus (-4D: -8D; +4D: -9.3D). This was not an artifact of the surgery, since there was no difference between Sham and ONS eyes before or 4 days after surgery, and ONS alone only induced -1.9D of myopia, far less than when combined with defocusing lenses (p<0.001). Interestingly, ONS eyes were able to recover from their myopia, losing 5D (-4D lens) or 6D (+4D lens) of their myopia, 15 days after lens removal.

Conclusions: : Mammalian eyes must depend on higher neural centers (or possibly ganglion cell activity) to respond appropriately to myopic defocus because ONS eyes were unable to inhibit their growth in response to plus spectacle lenses. Since recovery from myopia was intact after ONS, different mechanisms must underlie the inhibition of ocular growth when the eye is recovering from induced myopia compared to when the eye is slowing its natural emmetropisation. If human myopia arises from a failure in the slowing of ocular growth, then its development may also depend on visual activity extrinsic to the retina.1. Norton TT et al. 1994. Vis Neurosci. 11:143-53.2. McFadden SA 2002. IOVS 43: E-Abstract 18.3. Howlett MH, McFadden SA. 2008. Vision Res.

Keywords: myopia • optic nerve • emmetropization 

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