May 1999
Volume 40, Issue 6
Free
Articles  |   May 1999
Neuroprotective effects of eliprodil in retinal excitotoxicity and ischemia.
Author Affiliations
  • M A Kapin
    Retina/Degenerative Disease Research, Alcon Laboratories, Fort Worth, Texas 76134-2099, USA.
  • R Doshi
    Retina/Degenerative Disease Research, Alcon Laboratories, Fort Worth, Texas 76134-2099, USA.
  • B Scatton
    Retina/Degenerative Disease Research, Alcon Laboratories, Fort Worth, Texas 76134-2099, USA.
  • L M DeSantis
    Retina/Degenerative Disease Research, Alcon Laboratories, Fort Worth, Texas 76134-2099, USA.
  • M L Chandler
    Retina/Degenerative Disease Research, Alcon Laboratories, Fort Worth, Texas 76134-2099, USA.
Investigative Ophthalmology & Visual Science May 1999, Vol.40, 1177-1182. doi:
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    • Get Citation

      M A Kapin, R Doshi, B Scatton, L M DeSantis, M L Chandler; Neuroprotective effects of eliprodil in retinal excitotoxicity and ischemia.. Invest. Ophthalmol. Vis. Sci. 1999;40(6):1177-1182.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To evaluate whether eliprodil (SL82.0715), a NR2B-selective N-methyl-D-aspartate (NMDA) antagonist, is protective of retina subjected to an excitotoxic or ischemic insult. METHODS: To evaluate protection against retinal excitotoxicity, eliprodil was administered intraperitoneally before and after the injection of NMDA (5 microl, 20 nmol) into the vitreous of rats. Integrity of the retina was assessed by counting cells in the retinal ganglion cell layer (GCL) and measuring choline acetyltransferase (ChAT) activity. In a subsequent experiment, total retinal ischemia, as measured by a cessation of electroretinographic (ERG) activity, was induced in anesthetized rabbits by elevating intraocular pressure above systolic blood pressure for 65 minutes. After ischemia, recovery of ERG activity was assessed at 24 and 48 hours in animals treated with vehicle or eliprodil (1.0-10.0 mg/kg). RESULTS: Intravitreal NMDA injection resulted in a dose-related decrease in cells of the GCL and in ChAT activity. Eliprodil administered intraperitoneally at 10 mg/kg completely prevented the loss of ChAT and the loss of cells in the GCL. Twenty-four hours after retinal ischemia, A and B waves of vehicle-treated animals were suppressed by 60% to 70%. Eliprodil administered intraperitoneally at 10 mg/kg ameliorated the A- and B-wave depression throughout the 48-hour experiment. CONCLUSIONS: Eliprodil is neuroprotective of retinae subjected to either an excitotoxic or ischemic challenge and may be useful for treating a variety of retinal and optic nerve head disorders.

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