May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Retinal Transmitter Content Preceding Detectable Myopia Induced by Form Deprivation in Pigmented Mice
Author Affiliations & Notes
  • J. Tejedor
    Hospital Ramón y Cajal, Madrid, Spain
  • A. Clement
    Physiology, University of Alcalá, Alcalá de Henares, Spain
  • F. Germain
    Physiology, University of Alcalá, Alcalá de Henares, Spain
  • R. Martín del Río
    Hospital Ramón y Cajal, Madrid, Spain
  • P. de la Villa
    Physiology, University of Alcalá, Alcalá de Henares, Spain
  • Footnotes
    Commercial Relationships  J. Tejedor, None; A. Clement, None; F. Germain, None; R. Martín del Río, None; P. de la Villa, None.
  • Footnotes
    Support  ISCIII Grant PI040643, SAF Grant 04–5870–C02–01
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3321. doi:
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      J. Tejedor, A. Clement, F. Germain, R. Martín del Río, P. de la Villa; Retinal Transmitter Content Preceding Detectable Myopia Induced by Form Deprivation in Pigmented Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3321.

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

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Purpose: : To investigate the putative functional role of retinal neurotransmitters and glucagon in form deprivation myopia/anisometropia by neurochemical and immunocytochemical measurements of retinal content at suture removal (end of form–deprivation), before myopia is detectable.

Methods: : C57BL/6 mice were used. Left eyelids of animals were sutured at postnatal day 15 (P15) under 2% isoflurane anesthesia; after 2 weeks of form deprivation (P30), suture was removed and, following retinoscopic refraction, animals were sacrificed (5% isoflurane) and their eyes enucleated. Retinas were isolated, immersed in PBS 15% sulfosalicilic, and stored at –20ºC. Subsequently, retinas were homogenized and centrifuged, and the supernatant sample separated on a reversed–phase column HPLC–ED system to detect neurotransmitter levels. In another series of experiments, enucleated eyes were fixed in 4% paraformaldehyde, cryoprotected in PBS 20% sucrose, and 10–20 µm sections were obtained. Immunohistochemistry for a series of retinal neurotransmitters or neuromodulators (GABA, Glycine, Glutamate, and Glucagon) was carried out on retinal sections of deprived and control eyes. Quantitative and semiquantitative data of deprived and control eyes were compared (paired t and Wilcoxon test).

Results: : Retinoscopy demonstrated a relative hypermetropia at suture removal of form–deprived eyes (6.7 ± 5.3 D; mean ± SD, p= 0.04, paired t–test). Among all the neurotransmitters detected by the HPLC system (Aspartate, Glutamate, Glycine, GABA), significant differences were observed in Glycine (deprived/control eye ratio= 0.7, n= 45), and Aspartate (deprived/control eye ratio= 0.8, n= 45). Immunohystochemical experiments showed labeling of glucagon containing amacrine cells (GCAC) at dendritic processes and somas, and cell contacts between GCAC and GABAergic and glycinergic amacrine cells. Differences in labeling between control and deprived eyes were not clearly evident in quantitative estimation.

Conclusions: : Decreased content of Glycine observed in the retina of form–deprived mice, along with plausible decrease of Glucagon–like peptides derived from data of other species, may play a role in the pathophysiology of form–deprivation anisometropia/myopia.

Keywords: myopia • refractive error development 

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