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Neuroadaptations in Adenosine Receptor Signaling Following Long‐Term Ethanol Exposure and Withdrawal
Author(s) -
Butler Tracy R.,
Prendergast Mark A.
Publication year - 2012
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2011.01586.x
Subject(s) - adenosine , term (time) , neuroscience , pharmacology , adenosine receptor , receptor , chemistry , medicine , psychology , biochemistry , agonist , physics , quantum mechanics
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 A 1 and the A 2A 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 A 1 and the A 2A 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.