May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
REGULATION OF [3H]D–ASPARTATE RELEASE FROM PIG ISOLATED RETINAE BY PROSTAGLANDINS
Author Affiliations & Notes
  • K.H. Kulkarni
    College of Pharmacy, University of Houston, Houston, TX
  • K.L. Shivers
    College of Pharmacy, University of Houston, Houston, TX
  • E.M. Monjok
    College of Pharmacy, University of Houston, Houston, TX
  • C.A. Opere
    School of Pharmacy & Health Professions, Creighton University, Omaha, NE
  • S.E. Ohia
    College of Pharmacy, University of Houston, Houston, TX
  • Footnotes
    Commercial Relationships  K.H. Kulkarni, None; K.L. Shivers, None; E.M. Monjok, None; C.A. Opere, None; S.E. Ohia, None.
  • Footnotes
    Support  NIH Grant EY13266
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1037. doi:
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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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      © ARVO (1962-2015); The Authors (2016-present)

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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 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 
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