ArticleRole of acetaldehyde in the actions of ethanol on the brain — A review
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2019, Neuroscience of Alcohol: Mechanisms and TreatmentThe MAO-A inhibitor clorgyline reduces ethanol-induced locomotion and its volitional intake in mice
2014, Pharmacology Biochemistry and BehaviorCitation Excerpt :Acetaldehyde is a psychoactive molecule that, when administered centrally mimics with higher potency many of the behavioral (Arizzi-LaFrance et al., 2006; Rodd-Henricks et al., 2002; Sánchez-Catalán et al., 2009) and neurochemical (Diana et al., 2008; Enrico et al., 2009; Foddai et al., 2004) effects produced by EtOH in rodents, but with higher potency. For this reason, it has been postulated that this metabolite could be a mediator of some of the psychopharmacological properties of EtOH (Deitrich, 2004; Deng and Deitrich, 2008; Hipólito et al., 2007; Hunt, 1996; Quertemont et al., 2005; Smith et al., 1997). Thus, it has been demonstrated that many EtOH-related behaviors can be modified by altering the activity of the enzyme catalase in the CNS of rodents.
Influence of chronic ethanol intake on mouse synaptosomal aspartyl aminopeptidase and aminopeptidase A: Relationship with oxidative stress indicators
2012, AlcoholCitation Excerpt :This is probably due to free radicals which appear after chronic ethanol intake and are the direct consequence of ethanol action and independent from mitochondrial activity, as has been described by authors that postulate that chronic ethanol intake potentiates free radical generation in the nervous system (Montoliu, Valles, Renau-Piqueras, & Guerri, 1994; Mukherjee, Das, Vaidyanathan, & Vasudevan, 2008). In addition, chronic ethanol consumption may damage the nervous system directly via its oxidative metabolite acetaldehyde (Hunt, 1996) or through non-oxidative metabolites such as fatty acid ethyl esters (de Jersey & Treolar, 1994; Soderberg, Salem, Best, Cluette-Brown, & Laposata, 2003) or phosphatidylethanol (Dodd et al., 2000). The decrease of protein CGC levels after chronic ethanol intake could be a consequence of later modifications which are not related to neurotoxic events, such as structural alterations by enzymatic or non enzymatic glycosylation processes (Levine et al., 1990).
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2012, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Hence, in comparison with social drinking, ALD may have a more profound attention bias, and cause more profound executive and inhibition dysfunction. Other studies (Crews et al., 2005; Hunt, 1996) have reported that chronic exposure to ethanol may cause brain damage and generate an alteration in brain functions, mentality, and behavior in alcohol-dependent people. Hsiao et al. (2009) reported that BP-I and BP-II patients have different patterns of neuropsychological functioning, and that the neuropsychological function of the BP-II group could remit nearly to that of the HC group.