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Neuroadaptations in Adenosine Receptor Signaling Following Long-Term Ethanol Exposure and Withdrawal

Authors

  • Tracy R. Butler,

    1. From the Department of Psychology (TRB, MAP), Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky.
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  • Mark A. Prendergast

    1. From the Department of Psychology (TRB, MAP), Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky.
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Reprint requests: Tracy R. Butler, PhD, Department of Psychology, Spinal Cord and Brain Injury Research Center, B448D Biomedical and Biological Sciences Research Building, 741 South Limestone St., Lexington, KY 40536-0509; Tel.: 859-323-0575; Fax: 859-323-1979; E-mail: tracyrbutler@uky.edu

Abstract

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.

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