Purchase this article with an account.
C.A. Opere, K.H. Kulkarni, S.E. Ohia; Inhibitory Effect of Cannabinoids on [3H]D-aspartate Release from Bovine Isolated Retinae . Invest. Ophthalmol. Vis. Sci. 2003;44(13):5139.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: Although cannabinoid receptors are present in the mammalian retina (Lu et al., Vis. Neurosc. 17: 91, 2000), their role in neurocircuitry and neurotransmission remains unknown. In the present study, we evaluated the effect of cannabinoid CB-receptor agonists and antagonists on potassium (K+)-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 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: In the concentration range, 0.1 to 10 µM, the cannabinoid CB-receptor agonists methanandamide, arachidonyl-2'-chloroethylamide (ACEA) and WIN 55,212-2 caused a concentration-dependent inhibition of K+-induced [3H]D-aspartate overflow without affecting basal tritium efflux. For instance, at 10 µM, ACEA and methanadamide attenuated [3H]D-aspartate release by 37% and 20%, respectively. The cannabinoid CB1-receptor selective antagonist, N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251) completely reversed the effects of methanadamide (1 µM) and ACEA (1 µM) on K+-induced [3H]D-aspartate release. Conclusions: We conclude that CB1-receptors mediate the inhibitory action of cannabinoids on K+-induced [3H]D-aspartate release from bovine isolated retinae.
This PDF is available to Subscribers Only