title: Transient ischemia of the retina results in altered retrograde axoplasmic transport: neuroprotection with brimonidine.
abstract: In adult rats we have induced retinal ischemia and investigated retrograde axonal transport in ganglion cells. The animals received in their left eyes, 1 h prior to ischemia, two 5-microl drops of saline or 0.5% brimonidine (BMD). Retinal ischemia was induced by transient ligature of the left ophthalmic vessels for 90 min. One hour or 1 week after ischemia, Fluorogold (FG) was applied to both superior colliculi, the animals were processed 1 week after FG application, and FG-labeled retinal ganglion cell (RGC) densities were estimated in the right control and left experimental retinas. In the left retinas of the saline-pretreated animals, RGC densities diminished to 39 or 30% of the densities found in their right control retinas, 7 or 14 days after ischemia, respectively. Because in a previous similar study in which FG was applied 7 days before ischemia, the percentages of FG-labeled RGCs were 54 and 48%, 7 and 14 days after ischemia, respectively, this suggests that retrograde axonal transport was impaired in some surviving RGCs. This was confirmed in an additional group of rats in which 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate was applied to both SCi 3 weeks before ischemia, and FG was applied to the intraorbitally cut optic nerve 9 days after ischemia and 5 days before euthanization. In the left retinas of the BMD-pretreated animals, RGC densities amounted to 90% of the RGC population 7 or 14 days after ischemia and were comparable to those obtained in their contralateral nonischemic retinas. Retinal ischemia causes RGC loss and induces alterations of retrograde axonal transport in a proportion of surviving RGCs. BMD rescues RGCs from ischemia-induced cell death and preserves retrograde axonal transport in surviving RGCs.
authors.affiliation: Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Campus de Espinardo, E-30.100 Espinardo, Murcia, Spain.
authors.forename: María P
authors.initials: MP
authors.lastname: Lafuente López-Herrera
authors.forename: Sergio
authors.initials: S
authors.lastname: Mayor-Torroglosa
authors.forename: Jaime
authors.initials: J
authors.lastname: Miralles de Imperial
authors.forename: María P
authors.initials: MP
authors.lastname: Villegas-Pérez
authors.forename: Manuel
authors.initials: M
authors.lastname: Vidal-Sanz
mesh_terms: D000818:Animals; D001370:Axonal Transport / Q000187:drug effects / Q000502:physiology; D001369:Axons / Q000187:drug effects / Q000473:pathology*; D000068438:Brimonidine Tartrate; D005260:Female; D005456:Fluorescent Dyes / Q000493:pharmacokinetics; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000503:physiopathology*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D011810:Quinoxalines / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D005456:Fluorescent Dyes; D018696:Neuroprotective Agents; D011810:Quinoxalines; D000068438:Brimonidine Tartrate