April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Taurine Deficiency Damages Retinal Neurones, Cone Photoreceptors And Retinal Ganglion Cells
Author Affiliations & Notes
  • David Gaucher
    Ophthalmology, Hospital Civil de Strasbourg, Strasbourg, France
    Institut de la Vision, Paris, France
  • Emilie Arnault
    Institut de la Vision, Paris, France
  • Elisabeth Dubus
    Institut de la Vision, Paris, France
  • Julie Degardin
    Institut de la Vision, Paris, France
  • Manuel Simonutti
    Institut de la Vision, Paris, France
  • Tristan Bourcier
    Ophthalmology, Hospital Civil de Strasbourg, Strasbourg, France
  • Claude Speeg-Schatz
    Ophthalmology, Hospital Civil de Strasbourg, Strasbourg, France
  • Jose Alain Sahel
    Institut de la Vision, Paris, France
  • Serge Picaud
    Institut de la Vision, Paris, France
  • Footnotes
    Commercial Relationships  David Gaucher, None; Emilie Arnault, None; Elisabeth Dubus, None; Julie Degardin, None; Manuel Simonutti, None; Tristan Bourcier, None; Claude Speeg-Schatz, None; Jose Alain Sahel, None; Serge Picaud, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5436. doi:
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      David Gaucher, Emilie Arnault, Elisabeth Dubus, Julie Degardin, Manuel Simonutti, Tristan Bourcier, Claude Speeg-Schatz, Jose Alain Sahel, Serge Picaud; Taurine Deficiency Damages Retinal Neurones, Cone Photoreceptors And Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5436.

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

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Abstract
 
Purpose:
 

In the 80s,taurine deficiency was reported to induce photoreceptor degeneration in cats and rats. Recently we found that taurine deficiency contributes to the retinal toxicity of vigabatrin, an antiepileptic drug. However, in this toxicity, retinal ganglion cells (RGC) were degenerating in parallel to cone photoreceptors. The aim of this study was to re-assess a classic mouse model of taurine deficiency following a treatment with guanidoethane sulfonate (GES), a taurine transporter inhibitor to determine if retinal ganglion cells are also affected

 
Methods:
 

Taurine deficiency was induced by two months of GES oral treatment (0.1%) in 8 BALB / cJRj mice. Electroretinography (ERG), angiographic examinations using a scanning laser ophtalmoscope (SLO) and immunohistological studies were performed after treatment in GES mice and in 15 age-matched control mice.

 
Results:
 

GES treatment for 2 months induced a significant reduction in the taurine plasma levels and a lower weight increase. At the functional level, photopic electroretinograms were significantly reduced indicating a dysfunction in the cone pathway. A change in the autofluorescence appearance of the eye fundus was explained on histological sections by a increase autofluorescence of the retinal pigment epithelium. Although the general morphology of the retina was not affected, cell lesion was indicated by the general increase in GFAP expression. When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (19%) to the same amount as retinal ganglion cells (20%) (p<0.05). An abnormal synaptic plasticity of rod bipolar cell dendrites was also observed in GES treated mice.

 
Conclusions:
 

These results indicate that taurine deficiency can not only lead to photoreceptor degeneration but also retinal ganglion cell loss. Cone photoreceptor and retinal ganglion cells appear as the most sensitive cells to taurine deficiency. These results may explain the recent therapeutic interest of taurine in retinal degenerative pathologies, especially diabetic retinopathy.

 
Keywords: degenerations/dystrophies • neuroprotection • apoptosis/cell death 
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