Supported in part by the North Carolina Alcoholism Research Authority Grant 8605.
Effect of Acute Ethanol on Uptake of [3H]Adenosine by Rat Cerebellar Synaptosomes
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 13, Issue 3, pages 371–377, June 1989
How to Cite
Clark, M. and Dar, M. S. (1989), Effect of Acute Ethanol on Uptake of [3H]Adenosine by Rat Cerebellar Synaptosomes. Alcoholism: Clinical and Experimental Research, 13: 371–377. doi: 10.1111/j.1530-0277.1989.tb00338.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication May 19, 1988; revised manuscript received December 12, 1988: accepted December 16, 1988
Many classes of CNS-acting drugs have been suggested to act at least partially via inhibition of adenosine uptake. Synaptosomal uptake of [3H] adenosine and the effect of acute ethanol on it were studied in a rat brain area known to be involved in the coordination and modulation of normal motor activity, the cerebellum. Uptake of [3H] adenosine was found to be linear with time (about 40 sec) and increasing concentrations (up to 1.5 μM) of adenosine. The uptake of [3 H] adenosine was inhibited by dilazep (IC50= 2.5 × 10-7 M) in a dose-dependent manner. Pharmacologically and/or toxicologically relevant concentrations of ethanol (2.5 to 100 mM) significantly inhibited the uptake of [3 H] adenosine between 12 and 15%. Lineweaver-Burk plots indicated that both in vitro (25 mM) and in vivo (1.5 g/kg i.p.; 30 mM blood level) ethanol lowered Km as well as Vmax. values for adenosine uptake to nearly the same extent. In the case of in vivo ethanol, no ethanol was present during the assay since synaptosome preparation would wash out residual ethanol. The results of the present study indicate possible membranal alterations by in vivo ethanol. It is concluded that the uptake of [3 H] adenosine is inhibited by intoxicating concentrations of ethanol in vitro and by acute ethanol (1.5 g/kg) in vivo. This may partially explain the modulatory role of endogenous adenosine in ethanol-induced motor disturbances.