Dr. M. Clark is Biological Psychiatry Branch, National Institute of Mental Health, Bldg 10, Rm 3N212, Bethesda, MD 20892, U.S.A.
Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes
Version of Record online: 5 OCT 2006
Journal of Neurochemistry
Volume 52, Issue 6, pages 1859–1865, June 1989
How to Cite
Clark, M. and Dar, M. S. (1989), Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes. Journal of Neurochemistry, 52: 1859–1865. doi: 10.1111/j.1471-4159.1989.tb07268.x
- Issue online: 5 OCT 2006
- Version of Record online: 5 OCT 2006
- Received June 24, 1988; revised manuscript received November 9, 1988; accepted November 21, 1988
Abstract: The effects of pharmacologically relevant concentrations of ethanol on the release of endogenous adenosine from rat cerebellar synaptosomes were investigated. Release was conducted for 5, 10, 30, or 60 s after which time the incubation medium (containing the released adenosine) was rapidly separated from the synaptosomal membranes by vacuum filtration. The adenosine content of the filtrate was measured by HPLC–fluorescence detection. Both basal and KCl-stimulated adenosine release consisted of an initial rapid phase, for the first 10 s, that was followed by a relatively slower phase. Basal endogenous adenosine release was estimated as 199 ± 14 pmol/mg protein/5 s. Potassium (chloride) increased adenosine release from the basal level to 433 ± 83 pmol/mg protein/5 s. Ethanol caused a dose-dependent increase of adenosine release. The interaction between dilazep and ethanol indicates that ethanol-stimulated release does not involve the dilazep-sensitive transport system. The results support previous findings that indicate that cerebellar adenosine is involved in the mediation of ethanol-induced motor disturbances in the rat.