December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Effects of Anti-glaucoma Medications on Gangion Cell Survival: The DBA/2J Mouse Model
Author Affiliations & Notes
  • F Schuettauf
    Ophthalmology University Eye Hospital Tubingen Germany
  • R Naskar
    Experimental Ophthalmology University Eye Hospital Muenster Germany
  • KM Quinto
    Ophthalmology University of Pennsylvania Philadelphia PA
  • D Zurakowski
    Surgery and Biostatistics Children's Hospital Boston MA
  • Footnotes
    Commercial Relationships   F. Schuettauf, None; R. Naskar, None; K.M. Quinto, None; D. Zurakowski, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2186. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      F Schuettauf, R Naskar, KM Quinto, D Zurakowski; Effects of Anti-glaucoma Medications on Gangion Cell Survival: The DBA/2J Mouse Model . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2186.

      Download citation file:

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

  • Supplements

Abstract: : Purpose: Although various investigators have reported elevated intraocular pressure and glaucomatous changes in DBA/2J mice, they have not explored whether conventional glaucoma therapy could retard the ganglion cell loss in these animals, nor have they attempted to quantify ganglion cell survival in this mouse strain. Accordingly, we sought to determine whether several agents either approved or undergoing trials in human glaucoma - are effective at preventing ganglion cell loss in the DBA/2J mouse. Methods: Adult DBA/2J mice were either treated with commercial eye-drops containing timolol , pilocarpine, brimonidine, or dorzolamide, or received intraperitoneal injections of the NMDA-receptor antagonist memantine. Surviving retinal ganglion cells (RGC) of treated and control mice were retrogradely labeled with fluorogold and counted on retinal whole mounts. Results: In treated mice, memantine and timolol significantly increased the number of surviving RGC. Animals injected with memantine had 2316 ± 627 cells/mm² and eyes treated with timolol had 2313 ± 767 cells/mm² surviving six months after treatment. In contrast, eyes of mice subjected to treatment with dorzolamide had 1894 ± 456 cells/mm², eyes treated with pilocarpine had 1670 ± 1071 RGC/mm² surviving at six months. Untreated DBA/2J mice had 1652 ± 1064 retinal ganglion cells/mm² at six months. Conclusions: It appears that the DBA/2J mouse may represent a promising candidate for further experimentation in glaucoma, inasmuch as the DBA/2J disease process develops spontaneously, and leads to ganglion cell loss in a time dependent fashion. Our studies demonstrate that this time-dependent loss of RGC can be inhibited by either conventional anti-glaucomatous therapy with b-Blockers or injections with an NMDA-receptor antagonist. Hopefully, future work will establish whether lowering the IOP in this model is associated with the preservation of ganglion cells.


This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.