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Taurine deficiency damages retinal neurones: cone photoreceptors and retinal ganglion cells.

Gaucher D, Arnault E, Husson Z, Froger N, Dubus E, Gondouin P, Dherbécourt D, Degardin J, Simonutti M, Fouquet S, Benahmed MA, Elbayed K, Namer IJ, Massin P, Sahel JA, Picaud S - Amino Acids (2012)

Bottom Line: GES treatment induced a significant reduction in the taurine plasma levels and a lower weight increase.At the functional level, photopic electroretinograms were reduced indicating a dysfunction in the cone pathway.When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (20 %) as the number of retinal ganglion cells (19 %).

View Article: PubMed Central - PubMed

Affiliation: INSERM, U-968, Insitut de la Vision Retinal Information Processing: Pharmacology and Pathologies, 17, rue Moreau, 75012 Paris, France.

ABSTRACT
In 1970s, 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 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 whether retinal ganglion cells are also affected. GES treatment induced a significant reduction in the taurine plasma levels and a lower weight increase. At the functional level, photopic electroretinograms were reduced indicating a dysfunction in the cone pathway. A change in the autofluorescence appearance of the eye fundus was explained on histological sections by an increased autofluorescence of the retinal pigment epithelium. Although the general morphology of the retina was not affected, cell damages were indicated by the general increase in glial fibrillary acidic protein expression. When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (20 %) as the number of retinal ganglion cells (19 %). An abnormal synaptic plasticity of rod bipolar cell dendrites was also observed in GES-treated mice. These results indicate that taurine deficiency can not only lead to photoreceptor degeneration but also to retinal ganglion cell loss. Cone photoreceptors 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.

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Amacrine cells were not affected in GES mice. The density of amacrine cells did not differ between treated and untreated mice. In both groups (GES, a) (controls, b), amacrine cells were stained in red with anti-calretinin antibodies while GABA imunoreactive cells were stained in green with anti-GABA antibodies. GABA imunoreactive amacrine cells were co-labelled and appeared in yellow. Cell count did not show any difference in the density of both types of amacrine cells between the two groups of animals (c). Scale bars represent 50 μm (ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, RGCL retinal ganglion cell layer)
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Fig10: Amacrine cells were not affected in GES mice. The density of amacrine cells did not differ between treated and untreated mice. In both groups (GES, a) (controls, b), amacrine cells were stained in red with anti-calretinin antibodies while GABA imunoreactive cells were stained in green with anti-GABA antibodies. GABA imunoreactive amacrine cells were co-labelled and appeared in yellow. Cell count did not show any difference in the density of both types of amacrine cells between the two groups of animals (c). Scale bars represent 50 μm (ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, RGCL retinal ganglion cell layer)

Mentions: Finally, to investigate whether the retinal ganglion cell loss is related to an unspecific degeneration of the inner retina, we quantified two populations of amacrine cells, the calretinin immunopositive cells and the GABA-containing cells. In both cases, the difference was not statistically significant either between GES mice and control animals in calretinin-positive amacrine cells (GES group: 0.045 ± 0.006 cells/μm, SEM, n = 8; control group: 0.047 ± 0.003 cells/μm, SEM, n = 8, P > 0.05), or in GABA immunoreactive cells (GES group: 0.004 ± 0.001 cells/μm, SEM, n = 8; control: 0.005 cells/μm ± 0.002 SEM, n = 8, P > 0.05) (Fig. 10). These results demonstrated that the GES treatment and likely the consecutive taurine depletion triggered retinal ganglion cell degeneration.Fig. 10


Taurine deficiency damages retinal neurones: cone photoreceptors and retinal ganglion cells.

Gaucher D, Arnault E, Husson Z, Froger N, Dubus E, Gondouin P, Dherbécourt D, Degardin J, Simonutti M, Fouquet S, Benahmed MA, Elbayed K, Namer IJ, Massin P, Sahel JA, Picaud S - Amino Acids (2012)

Amacrine cells were not affected in GES mice. The density of amacrine cells did not differ between treated and untreated mice. In both groups (GES, a) (controls, b), amacrine cells were stained in red with anti-calretinin antibodies while GABA imunoreactive cells were stained in green with anti-GABA antibodies. GABA imunoreactive amacrine cells were co-labelled and appeared in yellow. Cell count did not show any difference in the density of both types of amacrine cells between the two groups of animals (c). Scale bars represent 50 μm (ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, RGCL retinal ganglion cell layer)
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3472058&req=5

Fig10: Amacrine cells were not affected in GES mice. The density of amacrine cells did not differ between treated and untreated mice. In both groups (GES, a) (controls, b), amacrine cells were stained in red with anti-calretinin antibodies while GABA imunoreactive cells were stained in green with anti-GABA antibodies. GABA imunoreactive amacrine cells were co-labelled and appeared in yellow. Cell count did not show any difference in the density of both types of amacrine cells between the two groups of animals (c). Scale bars represent 50 μm (ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, RGCL retinal ganglion cell layer)
Mentions: Finally, to investigate whether the retinal ganglion cell loss is related to an unspecific degeneration of the inner retina, we quantified two populations of amacrine cells, the calretinin immunopositive cells and the GABA-containing cells. In both cases, the difference was not statistically significant either between GES mice and control animals in calretinin-positive amacrine cells (GES group: 0.045 ± 0.006 cells/μm, SEM, n = 8; control group: 0.047 ± 0.003 cells/μm, SEM, n = 8, P > 0.05), or in GABA immunoreactive cells (GES group: 0.004 ± 0.001 cells/μm, SEM, n = 8; control: 0.005 cells/μm ± 0.002 SEM, n = 8, P > 0.05) (Fig. 10). These results demonstrated that the GES treatment and likely the consecutive taurine depletion triggered retinal ganglion cell degeneration.Fig. 10

Bottom Line: GES treatment induced a significant reduction in the taurine plasma levels and a lower weight increase.At the functional level, photopic electroretinograms were reduced indicating a dysfunction in the cone pathway.When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (20 %) as the number of retinal ganglion cells (19 %).

View Article: PubMed Central - PubMed

Affiliation: INSERM, U-968, Insitut de la Vision Retinal Information Processing: Pharmacology and Pathologies, 17, rue Moreau, 75012 Paris, France.

ABSTRACT
In 1970s, 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 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 whether retinal ganglion cells are also affected. GES treatment induced a significant reduction in the taurine plasma levels and a lower weight increase. At the functional level, photopic electroretinograms were reduced indicating a dysfunction in the cone pathway. A change in the autofluorescence appearance of the eye fundus was explained on histological sections by an increased autofluorescence of the retinal pigment epithelium. Although the general morphology of the retina was not affected, cell damages were indicated by the general increase in glial fibrillary acidic protein expression. When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (20 %) as the number of retinal ganglion cells (19 %). An abnormal synaptic plasticity of rod bipolar cell dendrites was also observed in GES-treated mice. These results indicate that taurine deficiency can not only lead to photoreceptor degeneration but also to retinal ganglion cell loss. Cone photoreceptors 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.

Show MeSH
Related in: MedlinePlus