Paper
1 April 1996 Pharmacological treatment of laser eye injuries by neuroprotection
Yoram Solberg M.D., Mordechai Rosner M.D., Michael Belkin M.D.
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Abstract
Many retinal injuries result in an irreversible neuronal loss, which can not yet be reduced by pharmacological methods. To determine whether glutamate-receptor blockers can serve as neuroprotective agents in the retina, as they do in the central nervous system, we examined the effects of MK-801, an NMDA-receptor antagonist, on laser-induced retinal injury in a rat model. Immediately and 8 h after argon laser retinal photocoagulation, rats were treated with intraperitoneal injections of MK-801 (3 mg/kg) or saline. After 3, 20 or 60 days the animals were sacrificed and their retinal lesions were evaluated histologically and morphometrically. Photoreceptor cell loss, both immediately and up to 2 months after laser irradiation, was significantly smaller in MK-801-treated rats than controls. MK-801 exhibits neuroprotective property in the retina. This points to the involvement of glutamate in the laser-induced retinal neuronal damage. Glutamate-receptor blockers should be further investigated for therapy of retinal diseases characterized by neuronal cell destruction.
© (1996) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.
Yoram Solberg M.D., Mordechai Rosner M.D., and Michael Belkin M.D. "Pharmacological treatment of laser eye injuries by neuroprotection", Proc. SPIE 2674, Laser-Inflicted Eye Injuries: Epidemiology, Prevention, and Treatment, (1 April 1996); https://doi.org/10.1117/12.237507
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KEYWORDS
Injuries

Control systems

Neurons

Retina

Laser irradiation

Eye

Argon ion lasers

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