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      Acetaldehyde involvement in ethanol's postabsortive effects during early ontogeny

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          Abstract

          Clinical and biomedical studies sustains the notion that early ontogeny is a vulnerable window to the impact of alcohol. Experiences with the drug during these stages increase latter disposition to prefer, use or abuse ethanol. This period of enhanced sensitivity to ethanol is accompanied by a high rate of activity in the central catalase system, which metabolizes ethanol in the brain. Acetaldehyde (ACD), the first oxidation product of ethanol, has been found to share many neurobehavioral effects with the drug. Cumulative evidence supports this notion in models employing adults. Nevertheless very few studies have been conducted to analyze the role of ACD in ethanol postabsorptive effects, in newborns or infant rats. In this work we review recent experimental literature that syndicates ACD as a mediator agent of reinforcing aspects of ethanol, during early ontogenetic stages. We also show a meta-analytical correlational approach that proposes how differences in the activity of brain catalase across ontogeny, could be modulating patterns of ethanol consumption.

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          Most cited references119

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          Age at onset of alcohol use and its association with DSM-IV alcohol abuse and dependence: results from the National Longitudinal Alcohol Epidemiologic Survey.

          Data from 27,616 current and former drinkers interviewed in the 1992 National Longitudinal Alcohol Epidemiologic Survey were used to examine the relationship between age at first use of alcohol and the prevalence of lifetime alcohol abuse and alcohol dependence, among all U.S. adults 18 years of age and over and within subgroups defined by sex and race. The rates of lifetime dependence declined from more than 40% among individuals who started drinking at ages 14 or younger to roughly 10% among those who started drinking at ages 20 and older. The rates of lifetime abuse declined from just over 11% among those who initiated use of alcohol at ages 16 or younger to approximately 4% among those whose onset of use was at ages 20 or older. After using multivariate logistic regression models to adjust for potential confounders, the odds of dependence decreased by 14% with each increasing year of age at onset of use, and the odds of abuse decreased by 8%. These findings are discussed with respect to their implications for prevention policies and the need to integrate epidemiological and intervention research.
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            The role of the dynorphin-kappa opioid system in the reinforcing effects of drugs of abuse.

            Initial hypotheses regarding the role of the kappa opioid system in drug addiction suggested that kappa receptor stimulation had anti-addictive effects. However, recent research suggests that kappa receptor antagonists may reverse motivational aspects of dependence. In the present review, we revisit the studies that measured the effects of kappa receptor ligands on the reinforcing and rewarding effects of drugs and postulate underlying neurobiological mechanisms for these effects to elaborate a more complex view of the role of kappa receptor ligands in drug addiction. The review of studies indicates that kappa receptor stimulation generally antagonizes the acute reinforcing/rewarding effects of drugs whereas kappa receptor blockade has no consistent effect. However, in a drug dependent-like state, kappa receptor blockade was effective in reducing increased drug intake. In animal models of reinstatement, kappa receptor stimulation can induce reinstatement via a stress-like mechanism. Results in conditioned place preference/aversion and intracranial self-stimulation indicate that kappa receptor agonists produce, respectively, aversive-like and dysphoric-like effects. Additionally, preclinical and postmortem studies show that administration or self-administration of cocaine, ethanol, and heroin activate the kappa opioid system. kappa receptor agonists antagonize the reinforcing/rewarding effects of drugs possibly through punishing/aversive-like effects and reinstate drug seeking through stress-like effects. Evidence suggests that abused drugs activate the kappa opioid system, which may play a key role in motivational aspects of dependence. Kappa opioid systems may have an important role in driving compulsive drug intake.
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              Pharmacological evidence for a motivational role of kappa-opioid systems in ethanol dependence.

              The purpose of this study was to test the hypothesis that activation of the dynorphin/kappa (kappa)-opioid system has a role in the increased consumption of ethanol in dependent animals. The effects of three opioid receptor antagonists with different effects on opioid receptors, naltrexone, nalmefene, and nor-binaltorphimine (nor-BNI), were compared in their ability to decrease ethanol self-administration in nondependent and ethanol-dependent male Wistar rats. Nalmefene and naltrexone are both opioid receptor ligands with comparable molecular weights and pharmacokinetic profiles, but differing specificity for the three opioid receptor subtypes at low doses, while nor-BNI is a selective kappa-opioid receptor antagonist. Dependence was induced in half the animals by subjecting them to a 4-week intermittent vapor exposure period in which animals were exposed to ethanol vapor for 14 h per day. Subsequent to dependence induction, nalmefene, naltrexone, and nor-BNI were tested for their ability to modulate self-administration of ethanol in vapor-exposed and control rats. The results indicated that both nalmefene and naltrexone induced a significant dose-dependent decrease in the number of lever presses for ethanol in both groups of animals. However, in ethanol-dependent animals, nalmefene was significantly more effective in suppressing ethanol intake than naltrexone. Nor-BNI selectively attenuated ethanol-dependent self-administration while leaving nondependent ethanol self-administration intact. Because naltrexone is primarily selective for the mu-opioid receptor, and nalmefene is primarily selective for the mu- and kappa-opioid receptor subtypes, the fact that nalmefene demonstrates more suppression in dependent animals suggests that opioid systems distinct from the mu-regulated portion may be involved in the increased drinking seen during withdrawal in dependent animals. The results with nor-BNI confirm that kappa-opioid receptor antagonism selectively decreases dependence-induced ethanol self-administration, which supports the hypothesis that dynorphin/kappa-opioid systems are dysregulated in dependence and contribute to the increased drinking seen during acute withdrawal in dependent rats.
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                Author and article information

                Journal
                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                1662-5153
                19 June 2013
                2013
                : 7
                : 70
                Affiliations
                [1] 1Laboratorio de Alcohol, Ontogenia y Desarrollo, Instituto de Investigación Médica Mercedes y Martín Ferreyra Córdoba, Argentina
                [2] 2Department de Psicología, Facultad de Psicología, Universidad Nacional de Córdoba Córdoba, Argentina
                Author notes

                Edited by: Merce Correa, Universitat Jaume, Spain

                Reviewed by: Merce Correa, Universitat Jaume, Spain; Sergey M. Zimatkin, Grodno State Medical University, Belarus; Marta Y. Pepino, Washington University School of Medicine, USA

                *Correspondence: Samanta M. March and Juan C. Molina, Laboratorio de Alcohol, Ontogenia y Desarrollo, Instituto de Investigación Médica Mercedes y Martín Ferreyra, Friuli 2434, PO Box 389, Córdoba, 5016, Argentina e-mail: smarch@ 123456immf.uncor.edu ; juancmolina2003@ 123456yahoo.com
                Article
                10.3389/fnbeh.2013.00070
                3685812
                23801947
                14d3e945-e487-401c-a815-b1e04b4bc860
                Copyright © 2013 March, Abate and Molina.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

                History
                : 20 March 2013
                : 01 June 2013
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 119, Pages: 8, Words: 7052
                Categories
                Neuroscience
                Mini Review Article

                Neurosciences
                early ethanol exposure,acetaldehyde,ontogeny,learning,appetitive response,suckling,newborns,infants

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