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Neuroprotection of retinal ganglion cells by brimonidine in rats with laser-induced chronic ocular hypertension.
Invest Ophthalmol Vis Sci. 2001 Nov; 42(12):2849-55.IO

Abstract

PURPOSE

To examine the neuroprotective effect of the alpha(2)-adrenergic agonist brimonidine in a chronic ocular hypertension model.

METHODS

Intraocular pressure (IOP) was elevated by laser photocoagulation of episcleral and limbal veins. Retinal ganglion cell loss was evaluated in wholemounted retinas. Brimonidine or timolol was administered, either at the time of or 10 days after IOP elevation and continued for 3 weeks. Drug-related immunohistochemical changes in glial fibrillary acidic protein (GFAP) were also determined after 3 weeks.

RESULTS

Laser treatment caused a twofold IOP increase over baseline that was maintained for 2 months. A time-dependent loss of ganglion cells occurred with elevated IOP. Systemic administration of brimonidine or timolol caused little decrease in IOP. After 3 weeks of elevated IOP, ganglion cell loss in control rats was 33% +/- 3%. Brimonidine reduced the progressive loss of ganglion cells to 26% +/- 1% and 15% +/- 2% at doses of 0.5 and 1 mg/kg. d, respectively. Timolol had no effect. Ten days of high IOP resulted in 22% +/- 4% ganglion cell loss. Brimonidine administration initiated 10 days after IOP elevation prevented any further loss of ganglion cells. In vehicle- or timolol-treated rats, ganglion cell loss continued to 33%. The increase in immunoreactivity of GFAP in ocular hypertensive retinas was attenuated by brimonidine.

CONCLUSIONS

Systemic application of brimonidine or timolol had little effect on IOP. Brimonidine, but not timolol, showed significant protection of retinal ganglion cells when applied at the time of IOP elevation and prevented further cell loss when applied after IOP was elevated. This indicates that brimonidine has a neuroprotective activity unrelated to its effect on ocular hypotension.

Authors+Show Affiliations

Department of Biological Sciences, Allergan Inc., Irvine, California 92612-1599, USA. woldemussie_liz@allergan.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11687528

Citation

WoldeMussie, E, et al. "Neuroprotection of Retinal Ganglion Cells By Brimonidine in Rats With Laser-induced Chronic Ocular Hypertension." Investigative Ophthalmology & Visual Science, vol. 42, no. 12, 2001, pp. 2849-55.
WoldeMussie E, Ruiz G, Wijono M, et al. Neuroprotection of retinal ganglion cells by brimonidine in rats with laser-induced chronic ocular hypertension. Invest Ophthalmol Vis Sci. 2001;42(12):2849-55.
WoldeMussie, E., Ruiz, G., Wijono, M., & Wheeler, L. A. (2001). Neuroprotection of retinal ganglion cells by brimonidine in rats with laser-induced chronic ocular hypertension. Investigative Ophthalmology & Visual Science, 42(12), 2849-55.
WoldeMussie E, et al. Neuroprotection of Retinal Ganglion Cells By Brimonidine in Rats With Laser-induced Chronic Ocular Hypertension. Invest Ophthalmol Vis Sci. 2001;42(12):2849-55. PubMed PMID: 11687528.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotection of retinal ganglion cells by brimonidine in rats with laser-induced chronic ocular hypertension. AU - WoldeMussie,E, AU - Ruiz,G, AU - Wijono,M, AU - Wheeler,L A, PY - 2001/11/1/pubmed PY - 2002/1/5/medline PY - 2001/11/1/entrez SP - 2849 EP - 55 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 42 IS - 12 N2 - PURPOSE: To examine the neuroprotective effect of the alpha(2)-adrenergic agonist brimonidine in a chronic ocular hypertension model. METHODS: Intraocular pressure (IOP) was elevated by laser photocoagulation of episcleral and limbal veins. Retinal ganglion cell loss was evaluated in wholemounted retinas. Brimonidine or timolol was administered, either at the time of or 10 days after IOP elevation and continued for 3 weeks. Drug-related immunohistochemical changes in glial fibrillary acidic protein (GFAP) were also determined after 3 weeks. RESULTS: Laser treatment caused a twofold IOP increase over baseline that was maintained for 2 months. A time-dependent loss of ganglion cells occurred with elevated IOP. Systemic administration of brimonidine or timolol caused little decrease in IOP. After 3 weeks of elevated IOP, ganglion cell loss in control rats was 33% +/- 3%. Brimonidine reduced the progressive loss of ganglion cells to 26% +/- 1% and 15% +/- 2% at doses of 0.5 and 1 mg/kg. d, respectively. Timolol had no effect. Ten days of high IOP resulted in 22% +/- 4% ganglion cell loss. Brimonidine administration initiated 10 days after IOP elevation prevented any further loss of ganglion cells. In vehicle- or timolol-treated rats, ganglion cell loss continued to 33%. The increase in immunoreactivity of GFAP in ocular hypertensive retinas was attenuated by brimonidine. CONCLUSIONS: Systemic application of brimonidine or timolol had little effect on IOP. Brimonidine, but not timolol, showed significant protection of retinal ganglion cells when applied at the time of IOP elevation and prevented further cell loss when applied after IOP was elevated. This indicates that brimonidine has a neuroprotective activity unrelated to its effect on ocular hypotension. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/11687528/Neuroprotection_of_retinal_ganglion_cells_by_brimonidine_in_rats_with_laser_induced_chronic_ocular_hypertension_ L2 - https://iovs.arvojournals.org/article.aspx?volume=42&issue=12&page=2849 DB - PRIME DP - Unbound Medicine ER -