REGULATION OF [3H]D–ASPARTATE RELEASE FROM PIG ISOLATED RETINAE BY PROSTAGLANDINS

Abstract

Abstract: : 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 PGF_2α 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.

Keywords: neurotransmitters/neurotransmitter systems • receptors: pharmacology/physiology • retina