May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Effect of Prostaglandins on Potassium–Evoked [3H]D–Aspartate Release From Bovine and Porcine Retinae, in vitro
Author Affiliations & Notes
  • M. Zhao
    Pharmacy Sciences, Creighton University, Omaha, NE
  • W. Zheng
    Pharmacy Sciences, Creighton University, Omaha, NE
  • K.K. Kaustubh
    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
    Pharmacy Sciences, Creighton University, Omaha, NE
  • S.E. Ohia
    College of Pharmacy, University of Houston, Houston, TX
  • Footnotes
    Commercial Relationships  M. Zhao, None; W. Zheng, None; K.K. Kaustubh, None; K.L. Shivers, None; E.M. Monjok, None; C.A. Opere, None; S.E. Ohia, None.
  • Footnotes
    Support  NIH Grant EY013967–01A1
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2229. doi:
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      M. Zhao, W. Zheng, K.K. Kaustubh, K.L. Shivers, E.M. Monjok, C.A. Opere, S.E. Ohia; Effect of Prostaglandins on Potassium–Evoked [3H]D–Aspartate Release From Bovine and Porcine Retinae, in vitro . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2229.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : In a previous study, we showed that prostaglandins (PGs) can inhibit electrically–evoked [3H]–dopamine release from isolated rabbit retinae via an effect on presynaptic EP3–receptors (Al–zadjali et al. Gen. Pharmac. 25: 289, 1994). It is, however, unclear if PGs can also regulate the release of excitatory amino acid neurotransmitters from mammalian retinae. Purpose: (i) To determine the effect of PGs on potassium (K+)–depolarization evoked [3H]D–aspartate release from the isolated, superfused bovine retina and (ii) to compare the effect of PGs on K+–depolarization evoked [3H]D–aspartate release from bovine and porcine retinae. 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 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: In the concentration range, 0.01 to 10 µM, PGE1, PGF sulprostone, misoprostone and fluprostenol caused a concentration–dependent inhibition of K+–evoked [3H]D–aspartate release from isolated, superfused bovine retinae without affecting basal tritium efflux. At a concentration that elicited 25% inhibition of K+–evoked [3H]D–aspartate overflow, the rank order of activity of prostanoids in bovine retinae was: fluprostenol > misoprostol > PGF2α = sulprostone > PGE1. In isolated porcine retinae, prostanoids also attenuated K+–evoked [3H]D–aspartate release with the following rank order of activity: sulprostone > PGE2 ≥ PGF> PGI2. In general, porcine retinae were more sensitive than their bovine counterparts to the inhibitory action of PGF, and sulprostone on K+–evoked [3H]D–aspartate. Conclusions: We conclude that PGs attenuate K+–evoked release of [3H]D–aspartate from isolated, superfused mammalian retinae in a species–specific manner.

Keywords: eicosanoids • excitatory neurotransmitters • retina 
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