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V.F. Roche, K.H. Kulkarni, K.L. Shivers, C.A. Opere, S.E. Ohia; EFFECT OF A BICYCLIC HEXAHYDROAPORPHINE ON POTASSIUM EVOKED [3H]D–ASPARTATE RELEASE FROM PORCINE ISOLATED RETINAE . Invest. Ophthalmol. Vis. Sci. 2004;45(13):439.
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© ARVO (1962-2015); The Authors (2016-present)
In a previous study, we reported that bicyclic hexahydroaporphines (HHAs) can lower intraocular pressure in normotensive rabbits in a dose–dependent fashion (Saha et al. J. Ocul. Pharmacol. Ther. 13: 497, 1997). Furthermore, we evidenced that HHAs can inhibit ischemia–induced [3H]D–aspartate release from isolated bovine retinae (Roche et al., ARVO abs. no. 3266, 2002). Purpose: To study the effect of nor–HHA on potassium (K+) depolarization evoked release of [3H]D–aspartate from isolated, superfused porcine retina. Methods: Isolated neural retinae were incubated in oxygenated Krebs solution containing 200nM of [3H]D–aspartate for 60 mins and then prepared for studies of neurotransmitter release using the superfusion method. Release of [3H]D–aspartate was evoked by an iso–osmotic concentration of K+(50 mM), with stimuli applied at 80–88 mins (S1) and 116–124 mins (S2) after the onset of superfusion. Nor–HHA was added to the buffer solution 12 mins before and during S2. Results: Exposure of retinae to successive K+–depolarizing stimuli caused an overflow of [3H]D–aspartate yielding S2/S1 ratios of unity. Nor–HHA (1 nM – 1 µM) caused a concentration–dependent inhibition of K+–depolarization without affecting basal tritium efflux. The highest concentration of nor–HHA (1 µM) tested elicited a 70% inhibition of K+–depolarization–evoked release of [3H]D–aspartate release. Conclusions: We conclude that nor–HHA produces an inhibitory action on evoked release of [3H]D–aspartate from porcine isolated retina.
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