Taurine deficiency damages photoreceptors and retinal ganglion cells in vigabatrin-treated neonatal rats

Mol Cell Neurosci. 2010 Apr;43(4):414-21. doi: 10.1016/j.mcn.2010.01.008. Epub 2010 Feb 1.

Abstract

The anti-epileptic drug vigabatrin induces an irreversible constriction of the visual field, but is still widely used to treat infantile spasms and some forms of epilepsy. We recently reported that vigabatrin-induced cone damage is due to a taurine deficiency. However, optic atrophy and thus retinal ganglion cell degeneration was also reported in children treated for infantile spasms. We here show in neonatal rats treated from postnatal days 4 to 29 that the vigabatrin treatment triggers not only cone photoreceptor damage, disorganisation of the photoreceptor layer and gliosis but also retinal ganglion cell loss. Furthermore, we demonstrate in these neonatal rats that taurine supplementation partially prevents these retinal lesions and in particular the retinal ganglion cell loss. These results provide the first evidence of retinal ganglion cell neuroprotection by taurine. They further confirm that taurine supplementation should be administered with the vigabatrin treatment for infantile spasms or epilepsy.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Analysis of Variance
  • Animals
  • Animals, Newborn
  • Anticonvulsants / pharmacology
  • Cell Count
  • Cell Death / drug effects*
  • Electroretinography
  • Fluorescent Antibody Technique
  • Neuroprotective Agents / administration & dosage
  • Optic Atrophy / chemically induced*
  • Optic Atrophy / pathology
  • Photoreceptor Cells / drug effects
  • Photoreceptor Cells / pathology*
  • Rats
  • Rats, Wistar
  • Retinal Ganglion Cells / drug effects
  • Retinal Ganglion Cells / pathology*
  • Taurine / administration & dosage
  • Taurine / deficiency*
  • Vigabatrin / pharmacology*

Substances

  • Anticonvulsants
  • Neuroprotective Agents
  • Taurine
  • Vigabatrin