title: Electroretinographical and histological study of mouse retina after optic nerve section: a comparison between wild-type and retinal degeneration 1 mice.
abstract: BACKGROUND
  Retinal ganglion cell death underlies the pathophysiology of neurodegenerative disorders such as glaucoma or optic nerve trauma. To assess the potential influence of photoreceptor degeneration on retinal ganglion cell survival, and to evaluate functionality, we took advantage of the optic nerve section mouse model.
  
  
  METHODS
  Surviving retinal ganglion cells were double-stained by exposing both superior colliculi to fluorogold, and by applying dextran-tetramethylrhodamine to the injured optic nerve stump. To assess retinal function in wild-type animals, electroretinograms were recorded on the injured eyes and compared with the contralateral. Similar labelling experiments were carried out on retinal degeneration 1 mice. Surviving retinal ganglion cells were counted 21 days after axotomy and compared with wild-type mice. No functional experiments were performed on retinal degeneration 1 animals because they do not develop normal electroretinographical responses.
  
  
  RESULTS
  A significant decrease in retinal ganglion cell density was observed 6 days after axotomy in the wild type. Functional studies revealed that, in scotopic conditions, axotomy induced a significant amplitude decrease in the positive scotopic threshold response component of the electroretinogram. Such decrease paralleled cell loss, suggesting it may be an appropriate technique to evaluate functionality. When comparing retinal ganglion cell densities in wild-type and retinal degeneration 1 mice, a significant greater survival was observed on the latter.
  
  
  CONCLUSIONS
  After optic nerve section, electroretinographical recordings exhibited a progressive decrease in the amplitude of the positive scotopic threshold response wave, reflecting ganglion cell loss. Interestingly, rod degeneration seemed, at least initially, to protect from axotomy-driven damage.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad de Alcalá, Madrid, Spain. francisco.germain@uah.es
authors.forename: Francisco
authors.initials: F
authors.lastname: Germain
authors.forename: Mirna
authors.initials: M
authors.lastname: Istillarte
authors.forename: Violeta
authors.initials: V
authors.lastname: Gómez-Vicente
authors.forename: Consuelo
authors.initials: C
authors.lastname: Pérez-Rico
authors.forename: Pedro
authors.initials: P
authors.lastname: de la Villa
mesh_terms: D000818:Animals; D019771:Axotomy; D002452:Cell Count; D016923:Cell Death; D002470:Cell Survival; D004195:Disease Models, Animal; D004596:Electroretinography; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D008817:Mice, Mutant Strains; D055254:Night Vision / Q000502:physiology; D009900:Optic Nerve / Q000502:physiology*; D009901:Optic Nerve Diseases / Q000175:diagnosis / Q000503:physiopathology*; D012160:Retina / Q000503:physiopathology*; D058499:Retinal Dystrophies / Q000175:diagnosis / Q000503:physiopathology*; D012165:Retinal Ganglion Cells / Q000473:pathology*; D013266:Stilbamidines
chemical_list: C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D013266:Stilbamidines
keywords: electroretinogram; optic neuropathy; retina; retinal degeneration