What is in that drink: the biological actions of ethanol, acetaldehyde, and salsolinol
- PMID: 22351424
- PMCID: PMC4955731
- DOI: 10.1007/7854_2011_198
What is in that drink: the biological actions of ethanol, acetaldehyde, and salsolinol
Abstract
Alcohol abuse and alcoholism represent substantial problems that affect a large portion of individuals throughout the world. Extensive research continues to be conducted in an effort to identify the biological basis of the reinforcing properties of alcohol in order to develop effective pharmacotherapeutic and behavioral interventions. One theory that has developed within the alcohol field over the past four decades postulates that the reinforcing properties of alcohol are due to the action of the metabolites/products of alcohol within the central nervous system (CNS). The most extreme version of this theory suggests that the biologically active metabolites/products of alcohol, created from the breakdown from alcohol, are the ultimate source of the reinforcing properties of alcohol. The contrary theory proposes that the reinforcing properties of alcohol are mediated completely through the interaction of the ethanol molecule with several neurochemical systems within the CNS. While there are scientific findings that offer support for both of these stances, the reinforcing properties of alcohol are most likely generated through a complex series of peripheral and central effects of both alcohol and its metabolites. Nonetheless, the development of a greater understanding for how the metabolites/products of alcohol contribute to the reinforcing properties of alcohol is an important factor in the development of efficacious pharmacotherapies for alcohol abuse and alcoholism. This chapter is intended to provide a historical perspective of the role of acetaldehyde (the first metabolite of alcohol) in alcohol reinforcement as well as review the basic research literature on the effects of acetaldehyde (and acetaldehyde metabolites/products) within the CNS and how these function with regard to alcohol reward.
Figures


Similar articles
-
Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol.Front Behav Neurosci. 2013 Aug 23;7:104. doi: 10.3389/fnbeh.2013.00104. eCollection 2013. Front Behav Neurosci. 2013. PMID: 23986666 Free PMC article.
-
The "first hit" toward alcohol reinforcement: role of ethanol metabolites.Alcohol Clin Exp Res. 2015 May;39(5):776-86. doi: 10.1111/acer.12709. Epub 2015 Apr 1. Alcohol Clin Exp Res. 2015. PMID: 25828063 Review.
-
A multi-dimensional examination of the positive reinforcing properties of acetaldehyde.Alcohol. 1985 Mar-Apr;2(2):367-70. doi: 10.1016/0741-8329(85)90077-1. Alcohol. 1985. PMID: 3893469 Review.
-
Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism.Mol Psychiatry. 2004 Jun;9(6):570-81. doi: 10.1038/sj.mp.4001497. Mol Psychiatry. 2004. PMID: 15164086 Review.
-
[What we drink when we drink? The role of the acetaldehyde in the alcohol consumption].Adicciones. 2007;19(1):5-11. Adicciones. 2007. PMID: 17687877 Spanish.
Cited by
-
Ethanol-derived acetaldehyde: pleasure and pain of alcohol mechanism of action.Front Behav Neurosci. 2013 Jul 17;7:87. doi: 10.3389/fnbeh.2013.00087. eCollection 2013. Front Behav Neurosci. 2013. PMID: 23882197 Free PMC article.
-
Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol.Front Behav Neurosci. 2013 Aug 23;7:104. doi: 10.3389/fnbeh.2013.00104. eCollection 2013. Front Behav Neurosci. 2013. PMID: 23986666 Free PMC article.
-
Hypothesizing Darkness Induced Alcohol Intake Linked to Dopaminergic Regulation of Brain Function.Psychology (Irvine). 2014 Mar;5(4):282-288. doi: 10.4236/psych.2014.54038. Psychology (Irvine). 2014. PMID: 25009759 Free PMC article.
-
Acetaldehyde and parkinsonism: role of CYP450 2E1.Front Behav Neurosci. 2013 Jun 21;7:71. doi: 10.3389/fnbeh.2013.00071. eCollection 2013. Front Behav Neurosci. 2013. PMID: 23801948 Free PMC article.
-
Modulation of Ethanol-Metabolizing Enzymes by Developmental Lead Exposure: Effects in Voluntary Ethanol Consumption.Front Behav Neurosci. 2017 May 23;11:95. doi: 10.3389/fnbeh.2017.00095. eCollection 2017. Front Behav Neurosci. 2017. PMID: 28588461 Free PMC article.
References
-
- Adell A, Myers RD. 5-HT, dopamine, norepinephrine, and related metabolites in brain of low alcohol drinking (LAD) rats shift after chronic intra-hippocampal infusion of harman. Neurochem Res. 1995;20:209–215. - PubMed
-
- Adell A, Myers RD. Increased alcohol intake in low alcohol drinking rats after chronic infusion of the beta-carboline harman into the hippocampus. Pharmacol Biochem Behav. 1994;49:949–953. - PubMed
-
- Airaksinen MM, Mahonen M, Tuomisto L, Peura P, Eriksson CJ. Tetrahydro-beta-carbolines: effect on alcohol intake in rats. Pharmacol Biochem Behav. 1983;18(Suppl 1):525–529. - PubMed
-
- Airaksinen MM, Saano V, Steidel E, Juvonen H, Huhtikangas A, Gynther J. Binding of beta-carbolines and tetrahydroisoquinolines by opiate receptors of the delta-type. Acta Pharmacol Toxicol (Copenh) 1984;55:380–385. - PubMed
-
- Alpers HS, McLaughlin, Nix WM, Davis VE. Inhibition of catecholamine uptake and retention in synaptosomal preparations by tetrahydroisoquinoline and tetrahydroprotoberberine alkaloids. Biochem Pharmacol. 1975;24:1391–1396.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Miscellaneous