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K.H. Kulkarni, K.L. Shivers, E.M. Monjok, C.A. Opere, S.E. Ohia; REGULATION OF [3H]D–ASPARTATE RELEASE FROM PIG ISOLATED RETINAE BY PROSTAGLANDINS . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1037.
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Prostaglandins (PGs) have been reported to regulate the release of neurotransmitters from both central and peripheral synapses. In the retina, we have evidence that PGs can inhibit electrically–evoked [3H]–dopamine release from the isolated rabbit retina by acting on presynaptic EP3–receptors (Al–zadjali et al. Gen. Pharmac. 25: 289, 1994). Purpose: (i) To study the effect of potassium (K+) depolarization on [3H]D–aspartate release from the isolated, superfused pig retina and (ii) to examine the effect of PGs on K+–depolarization evoked [3H]D–aspartate release from this tissue. Method: 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 iso–osmotic concentration of K+(50 mM) stimuli applied at 80–88 mins (S1) and 116–124 mins (S2) after the onset of superfusion. Results: Application of K+(50 mM) stimuli for eight minutes induced an overflow of [3H]D–aspartate over basal levels which can be repeated more than twice yielding S2/S1 ratios of 1.08 ± 0.08 (n = 7). In the concentration range, 0.1 to 100 µM, PGE2, PGI2 and PGF2α caused a concentration–dependent inhibition of K+–depolarization evoked [3H]D–aspartate release from isolated, superfused pig retinae without affecting basal tritium efflux. For instance, both PGE2 (3 µM) and PGI2 (1 µM) caused about 40% inhibition of the K+–induced [3H]D–aspartate overflow. Conclusion: We conclude that K+–depolarization can evoke the release of [3H]D–aspartate from isolated, superfused pig retinae. Furthermore, PGs produce an inhibitory effect on K+–depolarization induced release of radiolabeled D–aspartate from this tissue.
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