Amelioration of Light-Induced Retinal Degeneration by a Calcium Overload Blocker: Flunarizine

doi:10.1001/archopht.1991.01080040122042

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Vol. 109 No. 4, April 1991

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Amelioration of Light-Induced Retinal Degeneration by a Calcium Overload Blocker

Flunarizine

Deepak P. Edward, MD; Tim-Tak Lam, PhD; Shahin Shahinfar, MD; Junping Li, MD; Mark O. M. Tso, MD

Arch Ophthalmol. 1991;109(4):554-562.

Abstract

• Although free radical formation and lipid peroxidationhave been implicated in photoreceptor degeneration followingcontinuous light exposure, recent evidence led us to hypothesizethat excessive stimulation of the photoreceptor cells in prolongedlight exposure may cause intracellular calcium overload andconsequent photoreceptor cell injury. To test this hypothesis,we studied the effects of flunarizine hydrochloride, a calciumoverload blocker that inhibits the inositol 1,4,5-triphosphate-inducedrelease of intracellular stores of calcium, in an establishedrat model of light-induced retinal degeneration. Light and electronmicroscopic examination of the flunarizine-treated retinas revealedremarkable preservation of the retinal pigment epithelium, rodinner and outer segments, nuclei, and synapses of the photoreceptorcells at all phases of the recovery period. This observationwas further supported by morphometric evaluation of the outernuclear layer thickness, which revealed a greater preservationof the photoreceptor nuclei in the drug-treated animals at 6and 14 days after exposure. In addition, the rhodopsin levelsin the flunarizine-treated retinas were also significantly higherthan in the controls in all phases of recovery. The abilityof flunarizine to ameliorate light-induced retinal degenerationin the rat supports our hypothesis that elevated intracellularcalcium may indeed play a role in light-induced photoreceptordegeneration.

Author Affiliations

From the Georgiana Dvorak Theobald Ophthalmic Pathology Laboratory, Department of Ophthalmology, University of Illinois at Chicago College of Medicine.

Footnotes

Accepted for publication January 2, 1991.

Reprint requests to Georgiana Dvorak Theobald Ophthalmic PathologyLaboratory, Department of Ophthalmology, Lions of Illinois EyeResearch Institute, University of Illinois at Chicago Collegeof Medicine, 1855 W Taylor St, Chicago, IL 60612 (Dr Tso).

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