December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Inhibition of Ischemia-Induced [3H]D-Aspartate Release in Bovine Retinae by Cannabinoids
Author Affiliations & Notes
  • CA Opere
    Pharmacy Sciences Creighton University Omaha NE
  • AM LeDay
    Pharmacy Sciences Creighton University Omaha NE
  • KH Kulkarni
    Pharmacy Sciences Creighton University Omaha NE
  • SE Ohia
    Pharmacy Sciences Creighton University Omaha NE
  • Footnotes
    Commercial Relationships   C.A. Opere, None; A.M. LeDay, None; K.H. Kulkarni, None; S.E. Ohia, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1974. doi:
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      CA Opere, AM LeDay, KH Kulkarni, SE Ohia; Inhibition of Ischemia-Induced [3H]D-Aspartate Release in Bovine Retinae by Cannabinoids . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1974.

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

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Abstract: : Purpose: There is evidence that cannabinoid receptor agonists can protect rat hippocampal neurons against ischemia-induced, glutamate-mediated excitotoxicity (Nagayama et al., J. Neurosci. 19:2987, 1999). Although cannabinoid receptors subtypes have been localized in the mammalian retina (Lu et al., Vis. Neurosc. 17: 91, 2000), their role in neurocircuitry and neurotransmission is unknown. In the present study, we investigated the effect of selective cannabinoid CB1-receptor agonists on ischemia-induced [3H]D-aspartate release from bovine retinae in vitro. Methods: Isolated neural retinae were incubated in oxygenated Krebs solution containing 200 nM 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 K+(50 mM) stimuli applied at 90 mins (S1) and ischemia (induced by exposure of tissues to glucose-deficient Krebs buffer solution gassed with 95% N2:5% CO2) at 108 mins (S2) after the onset of superfusion. Under these experimental conditions, [3H]D-aspartate has been reported to be a valid marker of endogenous glutamate in retinal neurons (Santos et al., Neurochem. Res. 21: 361, 1996). Results: Under conditions of ischemia, the pO2 in glucose-deprived buffer solution was 0.54 ± 0.04 (n = 20). Exposure of bovine retinal tissues to ischemic buffer solution increased the spontaneous efflux of [3H]D-aspartate by 22%. In the concentration range, 0.1 µM to 1 µM, methananamide, a selective cannabinoid CB1-receptor agonist caused a concentration-dependent inhibition of ischemia-induced [3H]D-aspartate overflow without affecting basal tritium efflux. The IC50 (effective concentration of drug that caused 50% inhibition of the ischemic response) values obtained for methanandamide was 0.68 µM ± 0.1 (n = 4). Arachidonyl-2’-chloroethylamide (1 µM), another selective cannabinoid CB1-receptor agonist, also attenuated [3H]D-aspartate release by 30%. Conclusion: We conclude that selective cannabinoid CB1-receptor agonists can inhibit ischemia-induced [3H]D-aspartate release from bovine retinae. These compounds may have a neuroprotective role against glutamate excitotoxicity in the neural retina.

Keywords: 489 neuroprotection • 514 pharmacology • 556 retina: neurochemistry 

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