Urine methanol concentration and alcohol hangover severity
Congeners are substances, other than ethanol, that are produced during fermentation. Previous research found that the consumption of congener rich drinks contributes to the severity of alcohol hangover. Methanol is such a congener that has been related to alcohol hangover. Therefore, the aim of this study was to examine the relationship between urine methanol concentration and alcohol hangover severity. (Source: Alcohol)
Source: Alcohol - December 12, 2016 Category: Addiction Authors: M. Mackus, A.J.A.E. Van de Loo, G.A.H. Korte-Bouws, R.H.P. Van Neer, X. Wang, T.T. Nguyen, K.A. Brookhuis, J. Garssen, J.C. Verster Source Type: research
Cognitive sequelae of methanol poisoning involve executive dysfunction and memory impairment in cross-sectional and long-term perspective
Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13), 3–8 months after methanol poisoning and 57 control subjects (CS; age 49 ± 13) were administered a neuropsychological battery, 46 patients were followed in two years perspective. (Source: Alcohol)
Source: Alcohol - December 11, 2016 Category: Addiction Authors: O. Bezdicek, J. Michalec, M. Vaneckova, J. Klempir, I. Liskova, Z. Seidl, B. Janikova, M. Miovsky, J. Hubacek, P. Diblik, P. Kuthan, A. Pilin, I. Kurcova, Z. Fenclova, V. Petrik, T. Navratil, D. Pelclova, S. Zakharov, E. Ruzicka Source Type: research
Limbic circuitry activation in ethanol withdrawal is regulated by a chromosome 1 locus
Physiological dependence and associated withdrawal episodes are thought to constitute a motivational force sustaining alcohol use/abuse and contributing to relapse in alcoholics. Although no animal model exactly duplicates alcoholism, models for specific factors, including the withdrawal syndrome, are useful for identifying potential genetic and neural determinants of liability in humans. We previously identified highly significant quantitative trait loci (QTLs) with large effects on predisposition to withdrawal after chronic and acute alcohol exposure in mice and mapped these loci to the same region of chromosome 1 (Alcdp...
Source: Alcohol - December 6, 2016 Category: Addiction Authors: Kari J. Buck, Gang Chen, Laura B. Kozell Source Type: research
Effects of the serotonin transporter gene, sensitivity of response to alcohol, and parental monitoring on risk for problem alcohol use
The serotonin transporter-linked polymorphic region (5-HTTLPR) of the serotonin transporter gene (SLC6A4) has been previously associated with alcohol-related risk. Most findings point to short (S) allele carriers being at increased risk for negative alcohol outcomes relative to long allele homozygotes, although some work indicates a more complex relationship. The current prospective study aimed to clarify how and under what circumstances variations in 5-HTTLPR transmit risk for various alcohol-related outcomes. (Source: Alcohol)
Source: Alcohol - December 4, 2016 Category: Addiction Authors: Lora M. Cope, Emily C. Munier, Elisa M. Trucco, Jillian E. Hardee, Margit Burmeister, Robert A. Zucker, Mary M. Heitzeg Source Type: research
Binge alcohol consumption 18 h after induction of sepsis in a mouse model causes rapid overgrowth of bacteria, a cytokine storm, and decreased survival
Alcohol abuse increases vulnerability to infections and infection-related mortality. In previous studies, we found that acute alcohol abuse in a binge-drinking model in mice decreased resistance to bacterial sepsis when alcohol was administered near the time of bacterial challenge. In the present study, we investigated the effects of alcohol administered later in the course of sepsis (18 h after injection of Escherichia coli). Our working hypothesis was that decreased production of cytokines caused by alcohol at this time would actually improve survival, because overproduction of pro-inflammatory mediators is thought to ...
Source: Alcohol - November 25, 2016 Category: Addiction Authors: Minny Bhatty, Wei Tan, Maria D.S. Basco, Stephen Pruett, Bindu Nanduri Source Type: research
Resting state synchrony in long-term abstinent alcoholics: Effects of a current major depressive disorder diagnosis
Alcoholism is characterized by a lack of control over an impulsive and compulsive drive toward excessive alcohol consumption despite significant negative consequences; our previous work demonstrated that successful abstinence is characterized by decreased resting-state synchrony (RSS) as measured with functional magnetic resonance imaging (fMRI), within appetitive drive networks and increased RSS in emotion regulation and inhibitory executive control networks. Our hypothesis is that LTAA (Long-Term Abstinent Alcoholics) with a current major depressive disorder (MDD) drank primarily to deal with the negative affect associat...
Source: Alcohol - November 22, 2016 Category: Addiction Authors: George Fein, Jazmin Camchong, Valerie A. Cardenas, Andy Stenger Source Type: research
Initial subjective reward to alcohol in Sprague-Dawley rats
Initial subjective response to the rewarding properties of alcohol predicts voluntary consumption and the risk for alcohol use disorders. We assessed the initial subjective reward to alcohol in rats using a single exposure conditioned place preference (SE-CPP) paradigm. Sprague-Dawley rats demonstrate preference for a context paired with a single systemic injection of ethanol (1.0 g/kg, delivered intraperitoneally). However, expression of SE-CPP in males depended on pairing ethanol with the first exposure to the conditioning apparatus and procedures, while conditioning day did not appreciably affect SE-CPP in females, co...
Source: Alcohol - November 22, 2016 Category: Addiction Authors: Todd B. Nentwig, Kevin P. Myers, Judith E. Grisel Source Type: research
Preface to a special issue on genetic models of alcoholism and alcohol-stress interactions
This special issue of Alcohol brings together papers on mouse models of human alcohol use and abuse. Many of the papers have themes at the interface between alcoholism and the neurobiology of stress. Many are from members of the Integrative Neuroscience Initiative on Alcoholism (INIA) consortium —a large collaboration initiated by the National Institute on Alcohol Abuse and Alcoholism in 2002. These papers address some of the following questions: (1) What are the causal and mechanistic links between stressors and subsequent risk of alcoholism? (2) What genes, gene variants, and mechanisms account for highly variable resp...
Source: Alcohol - November 22, 2016 Category: Addiction Authors: Robert W. Williams, Andrew Holmes Source Type: research
Genetic Correlation between Alcohol Preference and Conditioned Fear: Exploring a Functional Relationship
Post-traumatic stress disorder (PTSD) and alcohol-use disorders have a high rate of co-occurrence, possibly because they are regulated by common genes. In support of this idea, mice selectively bred for high (HAP) alcohol preference show greater fear potentiated startle (FPS), a model for fear-related disorders such as PTSD, compared to mice selectively bred for low (LAP) alcohol preference. This positive genetic correlation between alcohol preference and FPS behavior suggests that the two traits may be functionally related. (Source: Alcohol)
Source: Alcohol - November 21, 2016 Category: Addiction Authors: Julia A. Chester, Marcus M. Weera Source Type: research
Long-term alterations to DNA methylation as a biomarker of prenatal alcohol exposure: From mouse models to human children with fetal alcohol spectrum disorders
Rodent models of Fetal Alcohol Spectrum Disorders (FASD) have revealed that prenatal alcohol exposure (PAE) results in differential DNA cytosine methylation in the developing brain. The resulting genome-wide methylation changes are enriched in genes with neurodevelopmental functions. The profile of differential methylation is dynamic and present in some form for life. The methylation changes are transmitted across subsequent mitotic divisions, where they are maintained and further modified over time. (Source: Alcohol)
Source: Alcohol - November 21, 2016 Category: Addiction Authors: Benjamin I. Laufer, Eric J. Chater-Diehl, Joachim Kapalanga, Shiva M. Singh Source Type: research
Involvement of Wnt pathway in ethanol-induced inhibition of mouse embryonic stem cell differentiation
Ethanol has been reported to have toxicity on embryonic stem cells (ESCs). The present study aims to address the teratogenic effects of ethanol on the growth and cardiac differentiation of ESCs. Mouse embryonic stem D3 cells were employed. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays were used to determine cytotoxicity. Quantitative real time polymerase chain reaction (qRT-PCR) and Western blotting were used to analyze the expressions of cardiac differentiation-related and Wnt signaling factors. (Source: Alcohol)
Source: Alcohol - November 15, 2016 Category: Addiction Authors: Qian Wang, Jing-wen Song, Yang Liu, Xian-xian Zhao Source Type: research
Developmental lead exposure induces opposite effects on ethanol intake and locomotion in response to central vs. systemic cyanamide administration
Lead (Pb) is a developmental neurotoxicant that elicits differential responses to drugs of abuse. Particularly, ethanol consumption has been demonstrated to be increased as a consequence of environmental Pb exposure, with catalase (CAT) and brain acetaldehyde (ACD, the first metabolite of ethanol) playing a role. The present study sought to interfere with ethanol metabolism by inhibiting ALDH2 (mitochondrial aldehyde dehydrogenase) activity in both liver and brain of control and Pb-exposed rats as a strategy to accumulate ACD, a substance that plays a major role in the drug's reinforcing and/or aversive effects. (Source: Alcohol)
Source: Alcohol - November 9, 2016 Category: Addiction Authors: Mara Soledad Mattalloni, Romina Deza-Ponzio, Paula Alejandra Albrecht, Liliana Marina Cancela, Miriam Beatriz Virgolini Source Type: research
Genome-wide analysis of the nucleus accumbens identifies DNA methylation signals differentiating low/binge from heavy alcohol drinking
Alcohol use disorders encompass a range of drinking levels and behaviors, including low, binge and heavy drinking. In this regard, investigating the neural state of individuals who chronically self-administer lower doses of alcohol may provide insight into mechanisms that prevent the escalation of alcohol use. DNA methylation is one of the epigenetic mechanisms that stabilizes adaptations in gene expression and has been associated with alcohol use. Thus, we investigated DNA methylation, gene expression and the predicted neural effects in the nucleus accumbens of male rhesus macaques categorized as “low” or “binge” ...
Source: Alcohol - November 9, 2016 Category: Addiction Authors: Rita Cervera-Juanes, Larry J. Wilhelm, Byung Park, Kathleen A. Grant, Betsy Ferguson Source Type: research
Initial genetic dissection of serum neuroactive steroids following chronic intermittent ethanol across BXD mouse strains
Neuroactive steroids modulate alcohol ’s impact on brain function and behavior. Ethanol exposure alters neuroactive steroid levels in rats, humans, and some mouse strains. We conducted an exploratoryanalysis of the neuroactive steroids (3α,5α)-3-hydroxypregnan-20-one (3α,5α-THP), (3α,5α)-3,21-dihydroxypregnan-20-one (3α,5α-THD OC), and pregnenolone across 126–158 individuals and 19 fully inbred strains belonging to the BXD family, which were subjected to air exposure, or chronic intermittent ethanol (CIE) exposure. (Source: Alcohol)
Source: Alcohol - November 8, 2016 Category: Addiction Authors: Patrizia Porcu, Todd K. O ’Buckley, Marcelo F. Lopez, Howard C. Becker, Michael F. Miles, Robert W. Williams, A. Leslie Morrow Source Type: research
DNA modifications in models of alcohol use disorders
Chronic alcohol use and abuse result in widespread changes to gene expression, some of which contribute to the development of alcohol use disorders (AUD). Gene expression is, in part, controlled by a group of regulatory systems often referred to as epigenetic factors, which includes, among other mechanisms, chemical marks made on the histone proteins around which genomic DNA is wound to form chromatin, and on nucleotides of the DNA itself. In particular, alcohol has been shown to perturb the epigenetic machinery, leading to changes in gene expression and cellular functions characteristic of AUD and, ultimately, to altered ...
Source: Alcohol - November 8, 2016 Category: Addiction Authors: Christopher T. Tulisiak, R. Adron Harris, Igor Ponomarev Source Type: research
