April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Influence of ON and OFF Pathways on Visual Function Development
Author Affiliations & Notes
  • Moe Hein Aung
    Neuroscience/Ophthalmology, Emory University, Atlanta, GA
  • Hanna Park
    Neuroscience/Ophthalmology, Emory University, Atlanta, GA
  • Curran S Sidhu
    Neuroscience/Ophthalmology, Emory University, Atlanta, GA
  • P Michael Iuvone
    Neuroscience/Ophthalmology, Emory University, Atlanta, GA
    Pharmacology, Emory University, Atlanta, GA
  • Machelle T Pardue
    Neuroscience/Ophthalmology, Emory University, Atlanta, GA
    Rehab R&D Center of Excellence, Atlanta VA Medical Center, Atlanta, GA
  • Footnotes
    Commercial Relationships Moe Aung, None; Hanna Park, None; Curran Sidhu, None; P Iuvone, None; Machelle Pardue, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 3513. doi:
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      Moe Hein Aung, Hanna Park, Curran S Sidhu, P Michael Iuvone, Machelle T Pardue; Influence of ON and OFF Pathways on Visual Function Development. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3513.

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

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Abstract

Purpose: ON and OFF pathways are essential components in visual discrimination. In this study, we evaluated the roles of ON and OFF pathways in mediating visual function during development using pathway-specific mutant mice.

Methods: Nob mice have a null mutation in the Nyx gene that encodes for the protein nyctalopin; this mutation results in lack of visual signal transmission in the retinal ON pathways. Alternatively, Vsx1 knockout (KO) mice have a null mutation in the visual system homeobox gene 1 (Vsx1), which leads to defects in the differentiation and function of most cone OFF bipolar cells and consequently defective OFF pathway signaling. With their respective wild-type controls (WT), C57BL/6 for nob and 129Sv for Vsx1 KO, we followed the development of visual acuity and peak contrast sensitivity weekly from 2 to 8 weeks of age using the virtual optokinetic system.

Results: Both nob and Vsx1 KO mice had significantly lower visual acuity levels than their WT counterparts early in development (p<0.05), with nob mice having more severe deficits than Vsx1 KO mice. Both nob and Vsx1 KO mice showed improvements in visual acuity thresholds that plateaued at similar thresholds as WT. However, nob mice did not reach WT levels until postnatal week 7, while Vsx1 KO mice were indistinguishable from WT starting at 3 weeks of age. Both nob and Vsx1 KO mice had consistently lower contrast sensitivities than their WT counterparts throughout the study period (p<0.001). Moreover, the spatial frequency that elicited maximal contrast sensitivity differed between the two WT strains (C57BL/6 vs. 129Sv).

Conclusions: Collectively, our results suggest that having a functional ON or OFF pathway is sufficient for normal visual acuity development by adulthood, but both pathways are necessary for proper contrast sensitivity perception. It would be interesting to determine if the differential effects of ON or OFF pathway defect on visual acuity and contrast sensitivity are due to differences in retinal dopamine content, a key modulator of the optokinetic response.

Keywords: 756 visual development • 502 dopamine • 693 retinal connections, networks, circuitry  
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