title: Intravitreal injection of ganglioside GM1 after ischemia reduces retinal damage in rats.
abstract: OBJECTIVE
  Gangliosides are normal components of cell membranes and contribute to structural rigidity and membrane function. They have been shown to protect against various insults in the brain. We have shown previously that GM1 administered intraperitoneally before the induction of retinal ischemia provides a protective effect. This study evaluates the protective effect of GM1 administered intravitreally after ischemia on retinal lesions.
  
  
  METHODS
  We induced retinal ischemia unilaterally in Long-Evans rats by increasing intraocular pressure to 160 mm Hg for 60 minutes. GM1 (20 microL x 10(-5) mol/L) or saline (20 microL) was injected into the vitreous 15 minutes after ischemia, and the postischemic survival time was either 8 or 15 days. The degree of retinal damage was assessed by histopathological study.
  
  
  RESULTS
  Retinal ischemia led to reductions in thickness and cell number, principally in the inner retinal layers (39% to 80%) and to a lesser extent in the outer retinal layers (26% to 45%). Postischemic treatment with intravitreally injected GM1 conferred significant protection against retinal ischemic damage after both 8 and 15 days of survival time. After 8 days of reperfusion, the ischemia-induced loss in overall retinal thickness was reduced by 15% and those of the inner nuclear and plexiform layers by 44% and 17%, respectively. Ischemic-induced ganglion cell and inner nuclear cell density losses were reduced by 37% and 27%, respectively. After 15 days of reperfusion, approximately the same statistically significant differences could be observed in comparison with the 15-day saline-injected group.
  
  
  CONCLUSIONS
  GM1 protects the rat retina from pressure-induced ischemic injury when given intravitreally after the insult. The protection provided by GM1 after initiation of retinal damage could be of therapeutic interest.
authors.affiliation: Laboratoire de Physiopathologie Retinienne, INSERM CJF 92-02, Universite Louis Pasteur, Strasbourg, France.
authors.forename: S
authors.initials: S
authors.lastname: Mohand-Said
authors.forename: M
authors.initials: M
authors.lastname: Weber
authors.forename: D
authors.initials: D
authors.lastname: Hicks
authors.forename: H
authors.initials: H
authors.lastname: Dreyfus
authors.forename: J A
authors.initials: JA
authors.lastname: Sahel
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005123:Eye / Q000098:blood supply* / Q000503:physiopathology / Q000648:ultrastructure; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D015427:Reperfusion Injury / Q000188:drug therapy*; D012160:Retina / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors; D014822:Vitreous Body
chemical_list: D018696:Neuroprotective Agents; D005677:G(M1) Ganglioside; D012965:Sodium Chloride