Abstract
Abstract: :
Purpose: Iganidipine is a water soluble Ca2+ channel blocker which can be prepared as ophthalmic solution. We have evaluated the neuroprotective effects of Iganidipine against glutamate receptors-mediated retinal damage in rat. Methods: NMDA (N-methyl-D-aspartic acid 200nmol) or KA(kainate acid 3nmol) was injected to vitreous of Male Sprague-Dawley rats to induce excitotoxic retinal ganglion cell (RGC) damage. The extent of RGC damage was evaluated by histological measurement of inner retinal cell layer thickness and by RGC counting with retrograde DiI labeling of RGCs. Iganidipine (6pmol,0.6pmol,o.06pmol) was injected with NMDA or KA intravitreously. As positive controls, MK801 (10nmol) or DNQX (6,7-dinitroquinoxaline-2,3-dione,0.125nmol) were injected intravitreously with NMDA or KA, respectively. The histlogical examination was performed seven days after the injection. For the RGC counting, DiI was injected into superior colliculi 5 days prior to the intravitreal injection of drugs for the retrograde labeling of RGCs and the number of labeled RGCs were counted microscopically 7 days after the injection. The other eye was used as control. Results: Intravitreal injection of NMDA reduced thickness of the inner plexiform layer (IPL) to 55±10% of control. Co-administration of MK801 with NMDA significantly prevented retinal damage (93±7% reduction) but iganidipine did not significantly prevent the NMDA-induced IPL thickness reduction. Intravitreal injection of KA reduced thickness of the inner plexiform layer (IPL) to 26±17% of control. Co-injection of 6pmol Iganidipine significantly prevented retinal damage (50±13 % reduction) along with co-administration of DNQX (93±7% reduction). Same results was seen in number of ganglion cells . Conclusion: Iganidipine partly prevents glutamate-induced neurotoxicity in rat retina .
Keywords: 489 neuroprotection • 334 calcium • 436 injection