Abstract
Abstract: :
Purpose: We examined the neuroprotective effect of lomerizine, a diphenylmethylpiperazine calcium channel blocker, on retinal ganglion cell (RGC) loss induced by optic nerve injury in the rat. Methods: Using a well-calibrated forceps, a crush lesion inflicted unilaterally on the optic nerve 2 mm behind the globe of adult Wistar albino rats. A sham operation was conducted to the contralateral eyes. The rats were randomly assigned into the following three groups: vehicle-treated group, and 10 or 30 mg / kg of lomerizine-treated group. Each drug was applied orally twice daily by a gastric tube until sacrifice. Intraocular pressure (IOP) was measured before and 7,14, and 28 days after acute optic nerve injury. One week before sacrifice, Fluoro-Gold (FG) was injected into the superior colliculi bilaterally to retrogradely stain surviving retinal ganglion cells (RGCs). Approximately one month after injury, retinal damage was assessed by counting FG-labeled RGCs and histologically. Results: In each group, IOP in crush eyes slightly elevated compared with sham-operated contralateral eyes during all follow-up periods. Within one month, in the control group the mean RGC density decreased to 65.9±3.5% of the contralateral eyes. Whereas, systemic applicalion of 10 mg / kg or 30 mg / kg of lomerizine significantly enhanced the RGC survival to 87.7±1.3% and 89.8±0.6%, respectively. Histological examinations showed no structural changes in each retinal layer in each group. Conclusions: Lomerizine might alleviate secondary degeneration of RGC induced by partial optic crush injury in the rat.
Keywords: animal model • pharmacology • neuroprotection