Neuroadaptations in Adenosine Receptor Signaling Following Long-Term Ethanol Exposure and Withdrawal
Article first published online: 18 JUL 2011
Copyright © 2011 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 36, Issue 1, pages 4–13, January 2012
How to Cite
Butler, T. R. and Prendergast, M. A. (2012), Neuroadaptations in Adenosine Receptor Signaling Following Long-Term Ethanol Exposure and Withdrawal. Alcoholism: Clinical and Experimental Research, 36: 4–13. doi: 10.1111/j.1530-0277.2011.01586.x
- Issue published online: 3 JAN 2012
- Article first published online: 18 JUL 2011
- Received for publication January 30, 2011; accepted April 27, 2011.
- Ethanol Withdrawal;
- A1 Receptor;
- A2A Receptor;
Ethanol affects the function of neurotransmitter systems, resulting in neuroadaptations that alter neural excitability. Adenosine is one such receptor system that is changed by ethanol exposure. The current review is focused on the A1 and the A2A receptor subtypes in the context of ethanol-related neuroadaptations and ethanol withdrawal because these subtypes (i) are activated by basal levels of adenosine, (ii) have been most well-studied for their role in neuroprotection and ethanol-related phenomena, and (iii) are the primary site of action for caffeine in the brain, a substance commonly ingested with ethanol. It is clear that alterations in adenosinergic signaling mediate many of the effects of acute ethanol administration, particularly with regard to motor function and sedation. Further, prolonged ethanol exposure has been shown to produce adaptations in the cell surface expression or function of both A1 and the A2A receptor subtypes, effects that likely promote neuronal excitability during ethanol withdrawal. As a whole, these findings demonstrate a significant role for ethanol-induced adaptations in adenosine receptor signaling that likely influence neuronal function, viability, and relapse to ethanol intake following abstinence.