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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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Taurine deficiency induces abnormal glial reactivity. The eyes sections were stained with DAPI and immunolabelled with anti-GFAP antibodies (a, b): glial reactivity was found in GES-treated mice as GFAP-positive processes extended vertically throughout the retina (a, c). The GFAP labelling was normally limited to the retinal ganglion cell layer and OPL in the control mice (b, d). Muller cells processes (red) extended to the outer limiting membrane, in contact with disorganized photoreceptors segments [stained in green with peanut lectin (PNA)] in GES-treated mice (c) as compared with controls (d)
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Fig6: Taurine deficiency induces abnormal glial reactivity. The eyes sections were stained with DAPI and immunolabelled with anti-GFAP antibodies (a, b): glial reactivity was found in GES-treated mice as GFAP-positive processes extended vertically throughout the retina (a, c). The GFAP labelling was normally limited to the retinal ganglion cell layer and OPL in the control mice (b, d). Muller cells processes (red) extended to the outer limiting membrane, in contact with disorganized photoreceptors segments [stained in green with peanut lectin (PNA)] in GES-treated mice (c) as compared with controls (d)

Mentions: The occurrence of retinal lesions is usually signed by retinal gliosis with increased expression of the GFAP (Wang et al. 2008; Jammoul et al. 2009). To assess whether retinal lesions were triggered by the GES treatment, retinal sections were therefore immunolabelled against GFAP. In control animals, GFAP expression was limited to the inner limiting membrane, whereas it extended throughout the retina in GES-treated animals from the inner limiting membrane to the outer limiting membrane (Fig. 6). These observations confirmed the presence of important retinal lesions in GES-treated animals.Fig. 6


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)

Taurine deficiency induces abnormal glial reactivity. The eyes sections were stained with DAPI and immunolabelled with anti-GFAP antibodies (a, b): glial reactivity was found in GES-treated mice as GFAP-positive processes extended vertically throughout the retina (a, c). The GFAP labelling was normally limited to the retinal ganglion cell layer and OPL in the control mice (b, d). Muller cells processes (red) extended to the outer limiting membrane, in contact with disorganized photoreceptors segments [stained in green with peanut lectin (PNA)] in GES-treated mice (c) as compared with controls (d)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3472058&req=5

Fig6: Taurine deficiency induces abnormal glial reactivity. The eyes sections were stained with DAPI and immunolabelled with anti-GFAP antibodies (a, b): glial reactivity was found in GES-treated mice as GFAP-positive processes extended vertically throughout the retina (a, c). The GFAP labelling was normally limited to the retinal ganglion cell layer and OPL in the control mice (b, d). Muller cells processes (red) extended to the outer limiting membrane, in contact with disorganized photoreceptors segments [stained in green with peanut lectin (PNA)] in GES-treated mice (c) as compared with controls (d)
Mentions: The occurrence of retinal lesions is usually signed by retinal gliosis with increased expression of the GFAP (Wang et al. 2008; Jammoul et al. 2009). To assess whether retinal lesions were triggered by the GES treatment, retinal sections were therefore immunolabelled against GFAP. In control animals, GFAP expression was limited to the inner limiting membrane, whereas it extended throughout the retina in GES-treated animals from the inner limiting membrane to the outer limiting membrane (Fig. 6). These observations confirmed the presence of important retinal lesions in GES-treated animals.Fig. 6

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