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Abstract
Abstract
Influence of Calpain Inhibitor III on Retinal Ganglion Cells in a Model of Intravitreal Excitotoxicity
Pallas M., Knop C., Behrens-Baumann W., Vorwerk C. K.
Dept. of Ophthalmology, Otto-von-Guericke University, Magdeburg
Purpose: The influence of an uncontrolled and prolonged calpain-mediated proteolysis has been suggested in the pathogenesis of neuronal cell death associated with excitotoxicity and ischemia. Traumatic or glaucomatous lesions of the optic nerve lead to a loss of retinal ganglion cells (RGC). The present study was initiated to determine if calpain inhibitor III could reduce the loss of RGC in a model of acute excitotoxic stimulation of RGC. Calpain inhibitor III has been shown to protect cultured neurons from NMDA and to offer neuroprotective effects in different models of cerebral ischemia.
Method: For all experiments adult Wistar rats were used. Excitotoxic lesions were induced by intraocular injection of 20 nmol NMDA, an endogenous glutamate agonist. A second group received in addition intraperitoneal injections of calpain inhibitor III (50 mg per kg body weight in Dimethyl-sulfoxide) 0, 3 and 6 hours after the intraocular NMDA lesion. 7 days after excitotoxic retinal damage RGC were labeled with fluorogold. After additional 2 days eyes were enucleated and retinal whole mounts counted for fluorogold positive RGC.
Results: RGC density in controls without lesion was 1855Zurück | Back