Alcohol RSS feed: Current Issue. Alcohol is an international, peer-reviewed journal that is devoted to publishing multi-disciplinary biomedical research on all aspects of the actions or effects of alcohol on the nervous system or on other organ systems. Emphasis is given to studies into the causes and consequences of alcohol abuse and alcoholism, and biomedical aspects of diagnosis, etiology, treatment or prevention of alcohol-related health effects. Intended for both research scientists and practicing clinicians, the journal publishes original research on the neurobiological, neurobehavioral, and pathophysiological processes associated with alcohol drinking, alcohol abuse, alcohol-seeking behavior, tolerance, dependence, withdrawal, protracted abstinence, and relapse. In addition, the journal reports studies on the effects alcohol on brain mechanisms of neuroplasticity over the life span, biological factors associated with adolescent alcohol abuse, pharmacotherapeutic strategies in the treatment of alcoholism, biological and biochemical markers of alcohol abuse and alcoholism, pathological effects of uncontrolled drinking, biomedical and molecular factors in the effects on liver, immune system, and other organ systems, and biomedical aspects of fetal alcohol spectrum disorder including mechanisms of damage, diagnosis and early detection, treatment, and prevention. Articles are published from all levels of biomedical inquiry, including the following: molecular and cellular studies of alcohol's actions in vitro and in vivo ; animal model studies of genetic, pharmacological, behavioral, developmental or pathophysiological aspects of alcohol; human studies of genetic, behavioral, cognitive, neuroimaging, or pathological aspects of alcohol drinking; clinical studies of diagnosis (including dual diagnosis), treatment, prevention, and epidemiology. The journal will publish 9 issues per year; the accepted abbreviation for Alcohol for bibliographic citation is Alcohol . Alcohol subscribes to the tenets of The Farmington Consensus (see http://www.elsevier.com/framework_products/promis_misc/525453fc.pdf or http://www1.elsevier.com/homepage/sab/alcohol/fconsensus.htm ). Submission of a paper to the journal will be taken as evidence that the authors have complied with the tenets set forth in the Consensus. All submitted material will be subject to peer review. Alcohol considers three types of manuscripts for publication: - Original research articles are full-length reports of the authors' original research addressing topics consistent with the Aims and Scope of the journal. Submissions outside the scope of the journal, or incomplete or fragmentary submissions, will not be considered. - Rapid communications are original, high-quality manuscripts that describe new data of high impact and major importance to the field. These contributions are typically short (e.g., 4 journal pages), and will be peer-reviewed by at least one expert in the field of the research and an Editor, and will be either accepted with minimal or no revisions or rejected. Publication of accepted rapid communications will be expedited. - Invited review articles will be considered for publication, upon invitation from the Editor-in-Chief, as full-length papers or mini-reviews. These contributions will be peer-reviewed. Contact the Editor-in-Chief concerning the suitability of a topic for an invited review. There are no page charges for articles published in Alcohol , and the current practice is to provide the corresponding author with 50 free reprints of his/her article. Effective May 2006, authors from all countries are invited to submit manuscripts, complete in all respects and following the Instructions to Authors (revised May 2006), to Charles R. Goodlett, Editor-in-Chief, via Elsevier electronic submission at http://ees.elsevier.com/alcohol Contact for questions: Charles R. Goodlett Editor-in-Chief, Alcohol Department of Psychology IUPUI 402 North Blackford Street Indianapolis, IN 46202-3275 Tel: +1-317 274-6772 Fax: +1-317 278-7181 E-mail: alcojrnl@iupui.edu http://www.alcoholjournal.org/?rss=yesElsevier Inc.en © 2010 Elsevier Inc. All rights reserved. Alcohol0741-8329441January 2010 © 2010 Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.alcoholjournal.org/article/PIIS0741832909002225/abstract?rss=yesI began drinking alcohol at the age of thirteen and gave it up in my fifty sixth year; it was like going straight from puberty to a mid-life crisis.—George Montgomery It is my pleasure to introduce this issue of Alcohol that is focused on the field of Adolescence and Alcohol. In my opinion, this is one of the most exciting fields of alcohol research and I am thankful to Drs Charles Goodlett and David Lovinger for allowing me the opportunity to guest edit this issue. I would also like to thank the many researchers who took time to add their valuable contributions to this issue and my hope is that the articles contained in this issue will serve as a catalyst for more research into understanding the effects of alcohol during this critical developmental period.Adolescence and alcohol: recent advances in understanding the impact of alcohol use during a critical developmental windowDouglas B. Matthews10.1016/j.alcohol.2009.10.018Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-812http://www.alcoholjournal.org/article/PIIS0741832909001955/abstract?rss=yesAbstract: It has been demonstrated by several laboratories that ethanol, both acute and chronic, produces effects that are age dependent. Specifically, adolescent rats are less sensitive to the hypnotic and motor-impairing effects of ethanol but are more sensitive to the hypothermic effects of the drug. However, the results on hippocampal function are not as clear. For example, there have been mixed findings regarding adolescent sensitivity of hippocampal-dependent (spatial) memory in response to ethanol. The current review explores the present state of the field as it relates to ethanol's effects in the hippocampus, particularly as it relates to spatial memory. In addition, we review potential neurobiological mechanisms that might underlie the age-dependent effects of ethanol in the hippocampus. Finally, future directions are proposed that will advance the state of the field as it relates to ethanol's effect during this developmental period.Effects of ethanol on hippocampal function during adolescence: a look at the past and thoughts on the futureVivien S. Chin, Candice E. Van Skike, Douglas B. Matthews10.1016/j.alcohol.2009.10.015Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-8314http://www.alcoholjournal.org/article/PIIS0741832909001712/abstract?rss=yesAbstract: Studies over the last decade demonstrate that adolescence is a brain maturation period from childhood to adulthood. Plastic and dynamic processes drive adolescent brain development, creating flexibility that allows the brain to refine itself, specialize, and sharpen its functions for specific demands. Maturing connections enable increased communication among brain regions, allowing greater integration and complexity. Compelling evidence has shown that the developing brain is vulnerable to the damaging effects of ethanol. It is possible to infer, therefore, that alcohol exposure during the critical adolescent developmental stages could disrupt the brain plasticity and maturation processes, resulting in behavioral and cognitive deficits. Recent neuroimaging studies have provided evidence of the impact of human adolescent drinking in brain structure and functions. Findings in experimental animals have also given new insight into the potential mechanisms of the toxic effects of ethanol on both adolescent brain maturation and the short- and long-term cognitive consequences of adolescent drinking.Adolescence is also characterized by the rapid maturation of brain systems mediating reward and by changes in the secretion of stress-related hormones, events that might participate in the increasing in anxiety and the initiation pattern of alcohol and drug consumption. Studies in human adolescents demonstrate that drinking at early ages can enhance the likelihood of developing alcohol-related problems. Experimental evidence suggests that early exposure to alcohol sensitizes the neurocircuitry of addiction and affects chromatin remodeling, events that could induce abnormal plasticity in reward–related learning processes that contribute to adolescents' vulnerability to drug addiction.In this article, we review the potential mechanisms by which ethanol impacts brain development and lead to brain impairments and cognitive and behavioral dysfunctions as well as the neurobiological and neurochemical processes underlying the adolescent-specific vulnerability to drug addiction.Mechanisms involved in the neurotoxic, cognitive, and neurobehavioral effects of alcohol consumption during adolescenceConsuelo Guerri, María Pascual10.1016/j.alcohol.2009.10.003Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-81526http://www.alcoholjournal.org/article/PIIS0741832909001682/abstract?rss=yesAbstract: This review discusses evidence for long-lasting neurophysiological changes that may occur following exposure to ethanol during adolescent development in animal models. Adolescence is the time that most individuals first experience ethanol exposure, and binge drinking is not uncommon during adolescence. If alcohol exposure is neurotoxic to the developing brain during adolescence, not unlike it is during fetal development, then understanding how ethanol affects the developing adolescent brain becomes a major public health issue. Adolescence is a critical time period when cognitive, emotional, and social maturation occurs and it is likely that ethanol exposure may affect these complex processes. To study the effects of ethanol on adolescent brain, animal models where the dose and time of exposure can be carefully controlled that closely mimic the human condition are needed. The studies reviewed provide evidence that demonstrates that relatively brief exposure to high levels of ethanol, via ethanol vapors, during a period corresponding to parts of adolescence in the rat is sufficient to cause long-lasting changes in functional brain activity. Disturbances in waking electroencephalogram and a reduction in the P3 component of the event-related potential (ERP) have been demonstrated in adult rats that were exposed to ethanol vapor during adolescence. Adolescent ethanol exposure was also found to produce long-lasting reductions in the mean duration of slow-wave sleep (SWS) episodes and the total amount of time spent in SWS, a finding consistent with a premature aging of sleep. Further studies are necessary to confirm these findings, in a range of strains, and to link those findings to the neuroanatomical and neurochemical mechanisms potentially underlying the lasting effects of adolescent ethanol exposure.Adolescent ethanol exposure: does it produce long-lasting electrophysiological effects?Cindy L. Ehlers, José R. Criado10.1016/j.alcohol.2009.09.033Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-82737http://www.alcoholjournal.org/article/PIIS074183290900216X/abstract?rss=yesAbstract: This review discusses the contributions of a newly considered form of plasticity, the ongoing production of new neurons from neural stem cells, or adult neurogenesis, within the context of neuropathologies that occur with excessive alcohol intake in the adolescents. Neural stem cells and adult neurogenesis are now thought to contribute to the structural integrity of the hippocampus, a limbic system region involved in learning, memory, behavioral control, and mood. In adolescents with alcohol use disorders (AUDs), the hippocampus appears to be particularly vulnerable to the neurodegenerative effects of alcohol, but the role of neural stem cells and adult neurogenesis in alcoholic neuropathology has only recently been considered. This review encompasses a brief overview of neural stem cells and the processes involved in adult neurogenesis, how neural stem cells are affected by alcohol, and possible differences in the neurogenic niche between adults and adolescents. Specifically, what is known about developmental differences in adult neurogenesis between the adult and adolescent is gleaned from the literature, as well as how alcohol affects this process differently among the age groups. Finally, this review suggests differences that may exist in the neurogenic niche between adults and adolescents and how these differences may contribute to the susceptibility of the adolescent hippocampus to damage. However, many more studies are needed to discern whether these developmental differences contribute to the vulnerability of the adolescent to developing an AUD.Roles of neural stem cells and adult neurogenesis in adolescent alcohol use disordersKimberly Nixon, Stephanie A. Morris, Daniel J. Liput, Matthew L. Kelso10.1016/j.alcohol.2009.11.001Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-83956http://www.alcoholjournal.org/article/PIIS0741832909001724/abstract?rss=yesAbstract: Alcohol use increases across adolescence and is a concern in the United States. In humans, males and females consume different amounts of alcohol depending on the age of initiation, and the long-term consequences of early ethanol consumption are not readily understood. The purpose of our work was to better understand the immediate and long-term impact of ethanol exposure during adolescence and the effects it can have on behavior and dopaminergic responsivity. We have assessed sex differences in voluntary ethanol consumption during adolescence and adulthood and the influence of binge ethanol exposure during adolescence. We have observed that males are sensitive to passive social influences that mediate voluntary ethanol consumption, and early ethanol exposure induces long-term changes in responsivity to ethanol in adulthood. Exposure to moderate doses of ethanol during adolescence produced alterations in dopamine in the nucleus accumbens septi during adolescence and later in adulthood. Taken together, all of these data indicate that the adolescent brain is sensitive to the impact of early ethanol exposure during this critical developmental period.Alcohol during adolescence selectively alters immediate and long-term behavior and neurochemistryAntoniette M. Maldonado-Devincci, Kimberly A. Badanich, Cheryl L. Kirstein10.1016/j.alcohol.2009.09.035Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-85766http://www.alcoholjournal.org/article/PIIS0741832909001700/abstract?rss=yesAbstract: The use of alcohol by adolescents is a growing problem and has become an important research topic in the etiology of the alcohol use disorders. A key component of this research has been the development of animal models of adolescent alcohol consumption and alcohol response. Because of their extended period of adolescence, rhesus macaques are especially well suited for modeling alcohol-related phenotypes that contribute to the adolescent propensity for alcohol consumption. In this review, we discuss studies from our laboratory that have investigated both the initial response to acute alcohol administration and the consumption of alcohol in voluntary self-administration paradigms in adolescent rhesus macaques. These studies confirm that adolescence is a time of dynamic change both behaviorally and physiologically, and that alcohol response and alcohol consumption are influenced by life history variables, such as age, sex, and adverse early experience in the form of peer-rearing. Furthermore, genetic variants that alter functioning of the serotonin, endogenous opioid, and corticotropin-releasing hormone systems are shown to influence both physiological and behavioral outcomes, in some cases interacting with early experience to indicate gene by environment interactions. These findings highlight several of the pathways involved in alcohol response and consumption, namely reward, behavioral dyscontrol, and vulnerability to stress, and demonstrate a role for these pathways during the early stages of alcohol exposure in adolescence.Alcohol response and consumption in adolescent rhesus macaques: life history and genetic influencesMelanie L. Schwandt, Stephen G. Lindell, Scott Chen, J. Dee Higley, Stephen J. Suomi, Markus Heilig, Christina S. Barr10.1016/j.alcohol.2009.09.034Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-86780http://www.alcoholjournal.org/article/PIIS0741832909001931/abstract?rss=yesAbstract: Animal and human studies have shown tolerance, consumption, relapse, and behavioral interactions between ethanol and nicotine, but little is understood about their interaction, especially as it relates to ethanol withdrawal in adulthood for subjects who have an adolescent history of using these drugs. This study investigated nicotine's influence on ethanol withdrawal seizures in two different age groups of male C3H mice. Adolescent and adult male C3H mice, beginning at postnatal day 28 or 70, respectively, were subjected to a 7-day chronic exposure to ethanol only, ethanol plus nicotine, nicotine only, or vehicle treatment. Six weeks later, all the groups were subjected to chronic exposure to ethanol vapors and the severity of their ethanol withdrawal seizures was assessed by handling-induced convulsions. An adolescent exposure to chronic nicotine resulted in an exacerbation of ethanol withdrawal seizures in adulthood. Given this, adolescence may contain a neurophysiological critical period that is sensitive to nicotine and which may result in an altered response to ethanol dependency in adulthood. These findings have serious implications for the long-term consequences following co-abuse of these drugs during adolescence.The influence of a chronic adolescent nicotine exposure on ethanol withdrawal severity during adulthood in C3H miceHugh H. Riley, André W. Zalud, Jaime L. Diaz-Granados10.1016/j.alcohol.2009.10.013Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-88187http://www.alcoholjournal.org/article/PIIS0741832909001979/abstract?rss=yesAbstract: Alcohol use during adolescence leads to increased risk of developing an alcohol use disorder (AUD) during adulthood. Converging evidence suggests that this period of enhanced vulnerability for developing an AUD may be due to the adolescent's unique sensitivity and response to alcohol. Adolescent rats have been shown to be less sensitive to alcohol intoxication and withdrawal susceptibility; however, age differences in ethanol pharmacokinetics may underlie these effects. Therefore, this study investigated alcohol intoxication behavior and withdrawal severity using a modified Majchrowicz model of alcohol dependence that has been shown to result in similar blood ethanol concentrations (BECs) despite age differences. Adolescent (postnatal day, PND, 35) and adult rats (PND 70+) received ethanol according to this 4-day binge paradigm and were observed for withdrawal behavior for 17h. As expected, adolescents showed decreased sensitivity to alcohol-induced CNS depression as evidenced by significantly lower intoxication scores. Thus, adolescents received significantly more ethanol each day (12.3±0.1g/kg/day) than adults (9.2±0.2g/kg/day). Despite greater ethanol dosing in adolescent rats, both adolescent and adult groups had comparable peak BECs (344.5±10.2 and 338.5±7.8mg/dL, respectively). Strikingly, withdrawal severity was similar quantitatively and qualitatively between adolescent and adult rats. Further, this is the first time that withdrawal behavior has been reported for adolescent rats using this model of alcohol dependence. A second experiment confirmed the similarity in BECs at various time points across the binge. These results demonstrate that after consideration of ethanol pharmacokinetics between adults and adolescents by using a model that produces similar BECs, withdrawal severity is nearly identical. This study, in combination with previous reports on ethanol withdrawal in adolescents and adults, suggests only a BEC-dependent effect of ethanol on withdrawal severity regardless of age.Similar withdrawal severity in adolescents and adults in a rat model of alcohol dependenceS.A. Morris, M.L. Kelso, D.J. Liput, S.A. Marshall, K. Nixon10.1016/j.alcohol.2009.10.017Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-88998http://www.alcoholjournal.org/article/PIIS0741832909001736/abstract?rss=yesAbstract: Ontogenetic studies using a social interaction paradigm have shown that adolescent rats are less sensitive to anxiolytic properties of acute ethanol than their adult counterparts. It is not known, however, whether adaptations to these anxiolytic effects on repeated experiences with ethanol would be similar in adolescents and adults. The present study investigated sensitivity to the anxiolytic effects of ethanol in adolescent and adult male and female Sprague–Dawley rats after 7 days of exposure (postnatal day [P] 27–33 for adolescents and P62–68 for adults) to 1g/kg ethanol or saline (intraperitoneally]) and in animals left nonmanipulated during this time. Anxiolytic effects of ethanol (0, 0.75, 1.0, 1.25, and 1.5g/kg for adolescents and 0, 0.25, 0.5, 0.75, 1.0, and 1.25g/kg for adults in experiments 1 and 2, respectively) were examined 48h after the last exposure using a modified social interaction test under unfamiliar test circumstances. At both ages, repeated ethanol exposure resulted in the development of apparent sensitization to anxiolytic effects of ethanol, indexed by enhancement of social investigation and transformation of social avoidance into social indifference or preference and expression of tolerance to the socially inhibiting effects induced by higher ethanol doses. Evidence for the emergence of sensitization in adults and tolerance at both ages was seen not only after chronic ethanol but also after chronic saline exposure, suggesting that chronic manipulation per se may be sufficient to alter the sensitivity of both adolescents and adults to socially relevant effects of ethanol.Sensitization to social anxiolytic effects of ethanol in adolescent and adult Sprague–Dawley rats after repeated ethanol exposureElena I. Varlinskaya, Linda P. Spear10.1016/j.alcohol.2009.09.036Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-899110http://www.alcoholjournal.org/article/PIIS0741832909001670/abstract?rss=yesAbstract: Binge alcohol use is common among teenagers with 28% of 12th graders reporting getting drunk in the past month. Chronic heavy drinking has been associated with verbal learning and memory deficits in adolescents and adults, yet verbal encoding in less frequently drinking teens has not yet been studied. Here, we examined functional magnetic resonance imaging (fMRI) response during verbal encoding among adolescent binge drinkers. Participants recruited from local high schools were of ages 16–18 and consisted of 12 binge drinkers and 12 demographically similar nondrinkers. Participants were all nonsmokers, and drinkers were abstinent from alcohol for an average of 33 days at the time of scanning. Participants performed a verbal paired associates learning task during fMRI acquisition. Drinkers recalled marginally fewer words than nondrinkers (P=.07). Compared with nondrinkers, bingers showed more response in right superior frontal and bilateral posterior parietal cortices but less response in occipital cortex during novel encoding (Ps 1,512μL). In addition, controls showed significant activation in the left hippocampus during novel encoding, whereas binge drinkers did not. Adolescent binge drinkers demonstrated (1) more response than nondrinkers in frontal and parietal regions, which could suggest greater engagement of working memory systems during encoding; (2) no hippocampal activation to novel word pairs; and (3) slightly poorer word pair recall, which could indicate disadvantaged processing of novel verbal information and a slower learning slope. Longitudinal studies will be needed to ascertain the degree to which emergence of binge drinking is linked temporally to these brain response patterns.A preliminary study of functional magnetic resonance imaging response during verbal encoding among adolescent binge drinkersAlecia D. Schweinsburg, Tim McQueeny, Bonnie J. Nagel, Lisa T. Eyler, Susan F. Tapert10.1016/j.alcohol.2009.09.032Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-8111117http://www.alcoholjournal.org/article/PIIS0741832909001669/abstract?rss=yesAbstract: In the past 15 years, both human and animal studies have advanced our understanding of the effects of adolescent alcohol exposure on behavioral and neural development, particularly in the areas of the ontogeny of initial sensitivity and tolerance to alcohol, the consequences of adolescent alcohol exposure on subsequent drinking patterns, as well as cognitive and neural function. Despite these advances, there are still substantial gaps in our understanding of whether heavy adolescent drinking interferes with normal brain development at the cellular and molecular level, and if so, how these changes may translate into patterns of brain connectivity that result in the emergence of alcohol use disorders. This article discusses our current knowledge of the cellular and molecular brain changes that stem from heavy alcohol exposure, including binge patterns, during adolescence. Progress has been made in linking the behavioral effects of adolescent drinking to underlying cellular and molecular mechanisms. However, it is suggested that future research on the etiology and consequences of adolescent drinking use an integrative approach to this problem by combining multiple levels, including genetic, cellular and molecular, systems (neuroimaging), and behavioral, with an emphasis on integrating the different levels of analysis.Research on alcohol and adolescent brain development: opportunities and future directionsEllen D. Witt10.1016/j.alcohol.2009.08.011Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-8119124http://www.alcoholjournal.org/article/PIIS0741832909002274/abstract?rss=yesTable of Contents10.1016/S0741-8329(09)00227-4Alcohol 44, 1 (2010)2010-01-01Alcohol2010-01-01441S0741-8329(09)X0010-8FrontmatterA3A3