Abstract
Currently, glaucoma is recognized as an optic neuropathy. Selective death of retinal ganglion cells (RGCs) is the hallmark of glaucoma, which is also associated with structural changes in the optic nerve head. Neuroprotection is an important issue in considering treatment options. Latanoprost, a prostaglandin F2α(PGF2α) analog prodrug, and unoprostone, an analog of a prostaglandin metabolite, have been shown to be effective in decreasing intraocular pressure when used alone or in combination with other ocular hypotensive agents. It is thought that a rise in intracellular calcium concentration is an inducement of cell death. Therefore , we investigated the suppressive effects of PGF2α on voltage-dependent Ca currents (ICa). Fast blue (FB) was injected into the superior colliculus of rats (7-12 days old) to identify RGCs under epifluorescence illumination after retrograde transport of FB to RGCs. Retinas were dissected, treated enzymatically, and dissociated with trituration. Effects of PGF2α on membrane currents at -90 mV and ICa were examined by whole-cell patch clamp method. ICa were recorded in the solution containing TTX(0.5μM), TEA (20mM) and 4AP (0.1mM) using an intracellular pipette containing CsCl2 (135mM). Currents recorded at -90 mV were not affected by PGF2α, whereas PGF2α reduced the peak component of the ICa reversibly by 14%. We suppose that the suppression of ICa by PGF2α may partly concern with therapeutic effects for glaucoma in preventing cell death in RGCs. [Jpn J Physiol 54 Suppl:S160 (2004)]
