Literature DB >> 2676355

Excitatory amino acids interfere with normal eye growth in posthatch chick.

M Barrington1, J Sattayasai, J Zappia, D Ehrlich.   

Abstract

This study examines the effects of excitotoxic amino acids on eye growth and retinal morphology. Day old chicks received a single intraocular injection of either 200 nmoles kainic acid (KA), 200 nmoles quisqualic acid (QUIS) or 400 nmoles N-methyl-D,L-aspartate (NMDA). Following survival periods of 7, 14 and 21 days, eyeballs were removed and weighed. Measurements of axial length, equatorial length, anterior chamber depth and corneal diameter were taken. Treatment with KA increased eye weight and equatorial length. Treatment with QUIS increased the anterior chamber depth but decreased the equatorial length. Treatment with NMDA increased anterior chamber depth, but to a lesser extent than QUIS. The effects of QUIS and NMDA could be distinguished from those of KA since the former excitotoxins resulted in a marked increase in anterior chamber depth with no enlargement of vitreal chamber. Changes in eye size were evident by day 7 and were sustained throughout the duration of the experiment. Examination of retinae revealed that KA lesions amacrine cells, bipolar cells, some ganglion cells and photoreceptors. Exposure to QUIS lesions amacrine cells, horizontal cells and causes mild disruption of photoreceptor outer segments. In contrast, NMDA predominantly lesions amacrine cells. The results demonstrate that these neurotoxins have different effects on eye growth, which may be associated with differences in retinal pathology. It is proposed that photoreceptors are ideally suited to play a role in the control of eye growth.

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Year:  1989        PMID: 2676355     DOI: 10.3109/02713688909000868

Source DB:  PubMed          Journal:  Curr Eye Res        ISSN: 0271-3683            Impact factor:   2.424


  6 in total

1.  Light modulation, not choroidal vasomotor action, is a regulator of refractive compensation to signed optical blur.

Authors:  Melanie J Murphy; David P Crewther; Melinda J Goodyear; Sheila G Crewther
Journal:  Br J Pharmacol       Date:  2011-11       Impact factor: 8.739

2.  Image defocus and altered retinal gene expression in chick: clues to the pathogenesis of ametropia.

Authors:  Richard A Stone; Alice M McGlinn; Donald A Baldwin; John W Tobias; P Michael Iuvone; Tejvir S Khurana
Journal:  Invest Ophthalmol Vis Sci       Date:  2011-07-29       Impact factor: 4.799

3.  Dopamine antagonists and brief vision distinguish lens-induced- and form-deprivation-induced myopia.

Authors:  Debora L Nickla; Kristen Totonelly
Journal:  Exp Eye Res       Date:  2011-08-23       Impact factor: 3.467

4.  Reprogramming retinal pigment epithelium to differentiate toward retinal neurons with Sox2.

Authors:  Wenxin Ma; Run-Tao Yan; Xiumei Li; Shu-Zhen Wang
Journal:  Stem Cells       Date:  2009-06       Impact factor: 6.277

5.  Ouabain inhibition of Na/K-ATPase across the retina prevents signed refractive compensation to lens-induced defocus, but not default ocular growth in young chicks.

Authors:  Melanie J Murphy; Sheila Gillard Crewther
Journal:  F1000Res       Date:  2013-03-28

6.  Neuroprotection by α2-Adrenergic Receptor Stimulation after Excitotoxic Retinal Injury: A Study of the Total Population of Retinal Ganglion Cells and Their Distribution in the Chicken Retina.

Authors:  Caridad Galindo-Romero; Mohammad Harun-Or-Rashid; Manuel Jiménez-López; Manuel Vidal-Sanz; Marta Agudo-Barriuso; Finn Hallböök
Journal:  PLoS One       Date:  2016-09-09       Impact factor: 3.240

  6 in total

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