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Current Eye Research Volume 31, 2006 - Issue 7-8
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Original Article

Inhibition of Potassium- and Ischemia-Evoked [3H] D-Aspartate Release from Isolated Bovine Retina by Cannabinoids

Catherine A. Opere Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University Medical Center, Omaha, Nebrasaka, USA
,
Wei Dong Zheng Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University Medical Center, Omaha, Nebrasaka, USA
,
Min Zhao Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University Medical Center, Omaha, Nebrasaka, USA
,
Jin Sook Lee Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University Medical Center, Omaha, Nebrasaka, USA
,
Kaustubh H. Kulkarni College of Pharmacy, University of Houston, Houston, Texas, USA
&
Sunny E. Ohia College of Pharmacy, University of Houston, Houston, Texas, USA
Pages 645-653 | Received 30 Jun 2005, Accepted 18 Apr 2006, Published online: 02 Jul 2009
 
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Abstract

We investigated the effect of cannabinoids on potassium chloride (K+)- and ischemia-induced [3H]D-aspartate release from isolated bovine retinae. The superfusion method was employed for studies of [3H]-neurotransmitter release. Cannabinoid receptor CB1 agonists, but not the CB2 agonist JWH 015, inhibited K+-induced [3H]D-aspartate release from bovine retinae with the following rank order of activity: anandamide > ACEA > methanandamide > WIN 55,212-2. In the ischemic model, the rank order of activity was as follows: methanandamide > ACEA > WIN 55,212-2. The CB1 receptor antagonist AM 251 blocked inhibitory responses produced by cannabinoids in both experimental conditions. In conclusion, cannabinoids inhibit evoked [3H]D-aspartate release from isolated bovine retinae via an effect on CB1 receptors.

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