The Role of Acetaldehyde in the Central Effects of Ethanol

Quertemont, Étienne; Grant, Kathleen A.; Correa, Mercè; Arizzi, Maria N.; Salamone, John D.; Tambour, Sophie; Aragón, Carlos M.G.; McBride, William J.; Rodd, Zachary A.; Goldstein, Avram; Zaffaroni, Alejandro; Li, Ting Kai; Pisano, Milena; Diana, Marco

doi:10.1097/01.alc.0000156185.39073.d2

Cited by 62 publications

(46 citation statements)

References 82 publications

(128 reference statements)

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“…Originally, it was postulated that peripheral ACD was unlikely to enter the CNS due to the prevalence of ALDH and the blood-brain barrier (Hunt, 1996). Further research indicated that high levels of peripherally administered ACD results in detection of ACD in the brain within minutes (Ward et al, 1997) Therefore, peripheral ACD may overwhelm the peripheral ALDH, allowing some percentage of ACD to enter the brain (Quertemont et al, 2005). Additional local metabolic pathways (e.g.…”

Section: Acetaldehyde Production In Cnsmentioning

confidence: 99%

What is in that Drink: The Biological Actions of Ethanol, Acetaldehyde, and Salsolinol

Deehan

Brodie

Rodd

2011

Behavioral Neurobiology of Alcohol Addiction

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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 4 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.

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Section: Acetaldehyde Production In Cnsmentioning

confidence: 99%

What is in that Drink: The Biological Actions of Ethanol, Acetaldehyde, and Salsolinol

Deehan

Brodie

Rodd

2011

Behavioral Neurobiology of Alcohol Addiction

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“…There is also extensive indirect evidence that AcH is responsible for a portion of the acute CNS effects of EtOH [reviewed in [13][14][15][16]17]. The issue addressed in this review is whether or not AcH may also play a role in tolerance and dependence of EtOH, hallmarks of "addiction".…”

Section: Introductionmentioning

confidence: 99%

Putative Role of Brain Acetaldehyde in Ethanol Addiction

Deng¹,

Deitrich²

2008

CDAR

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The putative contribution of brain acetaldehyde (AcH) to ethanol (EtOH) tolerance and dependence (addiction) is reviewed. Although the role of AcH in EtOH addiction has been controversial, there are data showing a relationship. AcH can be formed in the brain tissues through the peroxidatic activity of catalase and by oxidation via other oxidizing enzymes such as cytochrome P-4502E1. Significant formation of AcH occurs in vitro in brain tissue at concentrations of EtOH that can be achieved by voluntary consumption of EtOH by rodents. AcH itself possesses reinforcing properties, which suggests that some of the behavioral pharmacological effects attributed to EtOH may be a result of the formation of AcH, and supports the involvement of AcH in EtOH addiction. Modulation of aldehyde dehydrogenase (ALDH) and brain catalase activity can change EtOH-related addictive behaviors presumably by changing AcH levels. Moreover, some condensation reaction products of AcH may promote some actions of EtOH and its consumption. On the basis of the findings, it can be concluded that AcH may mediate some of the CNS actions of EtOH including tolerance and dependence, although further exploration the involvement of AcH in EtOH addiction is warranted.

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“…It has been suggested that some of the behavioral effects of ethanol are mediated by the first ethanol metabolite, acetaldehyde (Hunt 1996;Smith et al 1997;Quertemont et al 2005). Data suggesting a psychopharmacological significance for this ethanol metabolite was derived from two different approaches.…”

Section: Introductionmentioning

confidence: 99%