June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Antagonistic Effect of Ciliary and Superior Cervical Ganglion Sections on the Color and Luminance Emmetropization Mechanisms
Author Affiliations & Notes
  • Frances J Rucker
    Biomedical Science, New England Coll of Optometry, Boston, MA
  • Falk Schroedl
    Paracelsus Medical University, Salzburg, Austria
  • Footnotes
    Commercial Relationships Frances Rucker, None; Falk Schroedl, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2151. doi:
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      Frances J Rucker, Falk Schroedl, AP; Antagonistic Effect of Ciliary and Superior Cervical Ganglion Sections on the Color and Luminance Emmetropization Mechanisms. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2151.

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

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Purpose: Longitudinal chromatic aberration produces changes in retinal color and luminance contrast that guides emmetropization. An eye exposed to luminance contrast becomes hyperopic, like an atropine treated eye, an eye exposed to color contrast becomes more myopic. This experiment investigates the role of the autonomic nervous system in the control of emmetropization.

Methods: One to two week old, white leghorn chicks, underwent unilateral lesion of the ciliary ganglion (CGX; N=16) or superior cervical ganglion (SCGX; N=16). Animals were allowed to recover for one week, and were then placed in cages illuminated with sinusoidally modulated light (2 Hz: 80% contrast) that changed in luminance (LUM) contrast or COLOR (red to green) contrast (mean illumination 680 lux). Animals were kept in these illumination conditions for three days (9am-5pm), and otherwise in the dark. Changes in ocular components after the recovery period, and after exposure to the illuminants, were measured with OCT (Lenstar) and refraction with a Hartinger Refractometer. Changes in the lesioned eye were compared with the unlesioned fellow eye.

Results: After recovery: CGX produced an eye with relative hyperopia (2.01 ± 0.63D; p=0.006) and thinning of the anterior chamber (25 ± 11 µm; p=0.037). SCGX produced an enlarged eye (114 ± 26 µm; p<0.001) with longer vitreous chamber depth (154 ± 22 µm; p<0.001). With subsequent exposure to flicker: With CGX, LUM prevented significant eye growth (47 ± 30 µm) but the choroid thinned slightly (-17 ± 17 µm; p = 0.03) increasing vitreous depth (79 ± 17 µm; p < 0.01) without refractive shift (-1.1 ± 1.45 D; p = 0.44). The lens thickened (36 ± 8 µm; p = 0.002) and anterior chamber thinned (-41 ± 12 µm; p = 0.009). COLOR increased eye growth (101 ± 34 µm; p<0.05) but the choroid thickened (41 ± 19 µm), preventing significant vitreal (59 ± 33 µm) and refractive change (0.38 ± 1.0 D). <br /> With SCGX, LUM prevented vitreal growth (-13 ± 19 µm), and the choroid thickened slightly (16 ± 6 µm; p = 0.03), without refractive shift (0.3 ± 0.6 D). The lens thinned (32 ± 9 µm). COLOR increased vitreal growth (40 ± 14 µm; p=0.02) without refractive shift (0.8 ± 1.0 D).

Conclusions: The results indicate common neural pathways for CGX and LUM flicker, slowing growth and mostly affecting the anterior eye, and for SCGX and color flicker, increasing growth and affecting the posterior eye.


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