Alcohol (Fayetteville, N.Y.)

Publisher: Elsevier

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ISSN 1873-6823

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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: N-acetylcysteine (NAC), a glutamate-modulating agent with antioxidant and anti-inflammatory properties, has been considered as a potential anti-addictive drug. Beneficial effects were reported for cocaine, cannabis, and tobacco addicts, but the effect of NAC in alcoholics or in alcohol animal models is unknown. The aggravation of alcohol withdrawal symptoms, such as anxiety, has been associated with increased levels of serum corticosterone and leptin. Thus, the aim of this study was to assess the effects of NAC on anxiety, as well as corticosterone and leptin serum levels, after cessation of chronic alcohol treatment in rats. Male Wistar rats were treated with 2 g/kg ethanol, twice daily, by gavage for 30 days; control animals received an appropriate dose of glucose to balance caloric intake. Rats were treated for 4 days with NAC (60 and 90 mg/kg, intra-peritoneally [i.p.]) or saline after alcohol cessation. Twenty-four hours after the last treatment, rats were exposed to a 5-min session in the open-field test (OF). Corticosterone and leptin serum levels were determined by ELISA in samples collected within 30 min after the OF. Results showed that rats were hypoactive (decreased rearing, peripheral, and total crossings), and that corticosterone and leptin levels were increased 5 days after alcohol cessation. Four days of NAC prevented the behavioral and biochemical changes brought about by alcohol cessation. We suggest that, in addition to the anti-addictive properties reported for other drugs of abuse, NAC is potentially useful in the management of alcohol withdrawal. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 02/2015; DOI:10.1016/j.alcohol.2015.01.009
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    ABSTRACT: Alcohol withdrawal and therapies may affect nerve growth factor (NGF), brain-derived neurotrophic growth factor (BDNF), glial-derived neurotrophic growth factor (GDNF), and epinephrine (EPI). This study evaluated dexmedetomidine (DEX) on NGF, BDNF, GDNF, and EPI in severe alcohol withdrawal and related their plasma concentrations to DEX concentrations. Twenty-four subjects were randomized to DEX 1.2 mcg/kg/hour (high dose [HD]), 0.4 mcg/kg/hour (low dose [LD]), or placebo. Blood was collected at 0 (T0), 48 (T48), and 96-120 (T96) hours after starting the study drug, and concentrations of these transmitters and DEX were determined. Similar NGF suppression occurred at T48 and T96 across all groups. BDNF and GDNF levels increased insignificantly at T48 in the placebo group but steadily declined in both DEX groups, with a trend toward significance in the HD group at T48. EPI concentrations declined significantly in the HD group at T48, only to increase at T96. Median DEX concentrations during the study were insignificantly higher in HD than LD. T0 values of BDNF (r = -0.47, p = 0.02) and GDNF (r = -0.37, p = 0.05) were inversely associated with the need for mechanical ventilation before study enrollment. No other clinical parameter was associated with the plasma concentrations of these transmitters. Daily lorazepam requirements were associated with the severity of withdrawal (r = 0.7, p < 0.0001) and DEX concentrations were inversely related to daily lorazepam requirements (r = -0.33, p = 0.008). DEX utilization suppressed EPI (r = -0.57, p = 0.004). EPI concentrations were associated with BDNF values at T0 (r = 0.55, p = 0.04) and throughout the study (r = 0.25, p = 0.04). In summary, the plasma concentrations of NGF, BDNF, GDNF, and EPI during alcohol withdrawal are variable and the effects of DEX were marginal. DEX administration and higher DEX concentrations attenuated lorazepam administration in the short-term and suppressed EPI. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 02/2015; 49(1):15-9. DOI:10.1016/j.alcohol.2014.11.006
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    ABSTRACT: The central amygdala is a critical brain region for many aspects of alcohol dependence. Much of the work examining the mechanisms by which the central amygdala mediates the development of alcohol dependence has focused on the interaction of acute and chronic ethanol with central amygdala corticotropin releasing factor signaling. This work has led to a great deal of success in furthering the general understanding of central amygdala neurocircuitry and its role in alcohol dependence. Much of this work has primarily focused on the hypothesis that ethanol utilizes endogenous corticotropin releasing factor signaling to upregulate inhibitory GABAergic transmission in the central amygdala. Work that is more recent suggests that corticotropin releasing factor also plays an important role in mediating anxiety-like behaviors via the enhancement of central amygdala glutamatergic transmission, implying that ethanol/corticotropin releasing factor interactions may modulate excitatory neurotransmission in this brain region. In addition, a number of studies utilizing optogenetic strategies or transgenic mouse lines have begun to examine specific central amygdala neurocircuit dynamics and neuronal subpopulations to better understand overall central amygdala neurocircuitry and the role of neuronal subtypes in mediating anxiety-like behaviors. This review will provide a brief update on this literature and describe some potential future directions that may be important for the development of better treatments for alcohol addiction. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 01/2015; DOI:10.1016/j.alcohol.2015.01.006
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    ABSTRACT: The range of defects that fall within fetal alcohol spectrum disorder (FASD) includes persistent behavioral problems, with anxiety and depression being two of the more commonly reported issues. Previous studies of rodent FASD models suggest that interference with hypothalamic-pituitary-adrenal (HPA) axis structure and/or function may be the basis for some of the prenatal alcohol (ethanol) exposure (PAE)-induced behavioral abnormalities. Included among the previous investigations are those illustrating that maternal alcohol treatment limited to very early stages of pregnancy (i.e., gestational day [GD]7 in mice; equivalent to the third week post-fertilization in humans) can cause structural abnormalities in areas such as the hypothalamus, pituitary gland, and other forebrain regions integral to controlling stress and behavioral responses. The current investigation was designed to further examine the sequelae of prenatal alcohol insult at this early time period, with particular attention to HPA axis-associated functional changes in adult mice. The results of this study reveal that GD7 PAE in mice causes HPA axis dysfunction, with males and females showing elevated corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels, respectively, following a 15-min restraint stress exposure. Males also showed elevated CORT levels following an acute alcohol injection of 2.0 g/kg, while females displayed blunted ACTH levels. Furthermore, analysis showed that anxiety-like behavior was decreased after GD7 PAE in female mice, but was increased in male mice. Collectively, the results of this study show that early gestational alcohol exposure in mice alters long-term HPA axis activity and behavior in a sexually dimorphic manner. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 01/2015; DOI:10.1016/j.alcohol.2015.01.005
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    ABSTRACT: The present study compared two putative pharmacotherapies for alcohol abuse and dependence, dehydroepiandrosterone (DHEA) and pregnanolone, with two Food and Drug Administration (FDA)-approved pharmacotherapies, naltrexone and acamprosate. Experiment 1 assessed the effects of different doses of DHEA, pregnanolone, naltrexone, and acamprosate on both ethanol- and food-maintained responding under a multiple fixed-ratio (FR)-10 FR-20 schedule, respectively. Experiment 2 assessed the effects of different mean intervals of food presentation on responding for ethanol under a FR-10 variable-interval (VI) schedule, whereas Experiment 3 assessed the effects of a single dose of each drug under a FR-10 VI-80 schedule. In Experiment 1, all four drugs dose-dependently decreased response rate for both food and ethanol, although differences in the rate-decreasing effects were apparent among the drugs. DHEA and pregnanolone decreased ethanol-maintained responding more potently than food-maintained responding, whereas the reverse was true for naltrexone. Acamprosate decreased responding for both reinforcers with equal potency. In Experiment 2, different mean intervals of food presentation significantly affected the number of food reinforcers obtained per session; however, changes in the number of food reinforcements did not significantly affect responding for ethanol. Under the FR-10 VI-80 schedule in Experiment 3, only naltrexone significantly decreased both the dose of alcohol presented and blood ethanol concentration (BEC). Acamprosate and pregnanolone had no significant effects on any of the dependent measures, whereas DHEA significantly decreased BEC, but did not significantly decrease response rate or the dose presented. In summary, DHEA and pregnanolone decreased ethanol-maintained responding more potently than food-maintained responding under a multiple FR-10 FR-20 schedule, and were more selective for decreasing ethanol self-administration than either naltrexone or acamprosate under that schedule. Experiment 2 showed that ethanol intake was relatively independent of the interval of reinforcement in the food-maintained component, and Experiment 3 showed that naltrexone was the most effective drug at the doses tested when the interval for food reinforcement was low and maintained under a variable-interval schedule. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 01/2015; DOI:10.1016/j.alcohol.2014.07.024
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    ABSTRACT: The aim of the study is to determine the effect of acute alcohol consumption on enterocytes. Chronic alcohol consumption has been known to induce a decrease in gut wall integrity in actively drinking alcoholics and patients with alcohol-induced liver disease. Data on the extent of the damage induced by acute alcohol consumption in healthy human beings is scarce. Studies show that heavy incidental alcohol consumption is a growing problem in modern society. Data on this matter may provide insights into the consequences of this behavior for healthy individuals. In a randomized clinical trial in crossover design, 15 healthy volunteers consumed water one day and alcohol the other. One blood sample was collected pre-consumption, five every hour post-consumption, and one after 24 h. Intestinal fatty acid binding protein (I-FABP) was used as a marker for enterocyte damage. Liver fatty acid binding protein (L-FABP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) were used as markers for hepatocyte damage. Lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14) were used as a measure of translocation. Interleukin-6 (IL-6) was used to assess the acute inflammatory response to endotoxemia. Alcohol consumption caused a significant increase in serum I- and L-FABP levels, compared to water consumption. Levels increased directly post-consumption and decreased to normal levels within 4 h. LBP, sCD14, and IL-6 levels were not significantly higher in the alcohol group. Moderate acute alcohol consumption immediately damages the enterocyte but does not seem to cause endotoxemia. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 12/2014; DOI:10.1016/j.alcohol.2014.09.033
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    ABSTRACT: Blood alcohol is present in a third of trauma patients and has been associated with organ dysfunction. In both human studies and in animal models, it is clear that alcohol intoxication exerts immunomodulatory effects several hours to days after exposure, when blood alcohol is no longer detectable. The early immunomodulatory effects of alcohol while blood alcohol is still elevated are not well understood. Human volunteers achieved binge alcohol intoxication after high-dose alcohol consumption. Blood was collected for analysis prior to alcohol ingestion, and 20 min, 2 h, and 5 h after alcohol ingestion. Flow cytometry was performed on isolated peripheral blood mononuclear cells, and cytokine generation in whole blood was measured by enzyme-linked immunosorbent assay (ELISA) after 24-h stimulation with lipopolysaccharide (LPS) and phytohemagglutinin-M (PHA) stimulation. An early pro-inflammatory state was evident at 20 min when blood alcohol levels were ∼130 mg/dL, which was characterized by an increase in total circulating leukocytes, monocytes, and natural killer cells. During this time, a transient increase in LPS-induced tumor necrosis factor (TNF)-α levels and enhanced LPS sensitivity occurred. At 2 and 5 h post-alcohol binge, an anti-inflammatory state was shown with reduced numbers of circulating monocytes and natural killer cells, attenuated LPS-induced interleukin (IL)-1β levels, and a trend toward increased interleukin (IL)-10 levels. A single episode of binge alcohol intoxication exerted effects on the immune system that caused an early and transient pro-inflammatory state followed by an anti-inflammatory state. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 12/2014; 49(1). DOI:10.1016/j.alcohol.2014.10.002
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    ABSTRACT: Excessive alcohol use and non-alcoholic fatty liver disease (NAFLD) are putative cardiovascular disease risk factors. In order to ease the identification of these conditions on primary health care level, we aimed to determine and compare the demographic and cardiometabolic characteristics of excessive alcohol users and those with suspected NAFLD in black South Africans. In the Prospective Urban Rural Epidemiology study (North West Province, South Africa, N = 2021, collected in 2005) we selected 338 participants, namely: 1) alcohol users (N = 143) reporting 'yes' to alcohol intake, with high gamma-glutamyl transferase (GGT) ≥80 U/L and a percentage carbohydrate deficient transferrin (%CDT) ≥2%; 2) non-alcohol users (N = 127) self-reporting 'no' to alcohol intake with GGT ≤30 U/L and %CDT ≤2%; and 3) NAFLD group (N = 68) who were non-drinkers with GGT levels ≥60 U/L and %CDT ≤ 2%. The demographics indicated that the alcohol users were mostly men (73%) with a body mass index (BMI) of 19.8 (15.2-27.3) kg/m(2), 90% of which were smokers. Systolic blood pressure (SBP) of alcohol users significantly correlated with high-density lipoprotein cholesterol (HDL-C) (β = 0.24; p = 0.003) and waist circumference (WC) (β = 0.22; p = 0.006). Non-alcohol users were mostly women (84%) with a BMI of 26.0 (18.0-39.2) kg/m(2) and blood pressure in this group related positively with triglycerides. The NAFLD group were also mostly women (72%) with a comparatively larger WC (p < 0.001) and an adverse metabolic profile (total cholesterol: 5.55 ± 1.69 mmol/L; glycosylated hemoglobin: 6.03 (4.70-9.40) %). Diastolic blood pressure in the NAFLD group associated positively with WC (β = 0.27; p = 0.018). We therefore found disparate gender and cardiometabolic profiles of black South Africans with suspected NAFLD and excessive alcohol use. The described profiles may aid health care practitioners in low resource settings when using these crude screening measures of gender, obesity indices (and self-reported alcohol use) to identify individuals at risk. Copyright © 2014 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 12/2014; 49(2). DOI:10.1016/j.alcohol.2014.11.002
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    ABSTRACT: Alcohol use disorders and anxiety disorders are highly comorbid in humans. In rodent lines selected for alcohol drinking, differences in anxiety-like behavior are also seen. The High Drinking in the Dark (HDID) lines of mice are selectively bred for drinking to intoxication during limited access to alcohol, and these mice represent a genetic model of risk for binge-like drinking. The present studies investigated whether these selected lines differ from control (HS) mice in basal anxiety behavior or in anxiolytic response to alcohol. We also assessed the genetic correlation between alcohol drinking in the dark (DID) and basal anxiety-like behavior using existing inbred strain data. Mice of both sexes and HDID replicates (HDID-1 and HDID-2) were tested on an elevated zero maze immediately following a DID test. In general, HDID mice showed more time spent in the open arms after drinking alcohol than HS mice, and open-arm time was significantly correlated with blood alcohol concentration. HDID-1 male mice also showed less anxiety-like behavior at baseline (water-drinking controls). In a separate experiment, HDID-1 and HS mice were tested for anxiolytic dose-response to acute alcohol injections. Both genotypes showed increasing time spent in the open arms with increasing alcohol doses, and HDID-1 and female mice had greater open-arm time across all doses. HDID-1 control males showed lower anxiety-like behavior than the HS control males. Inbred strain data analysis also showed no significant genetic relationship between alcohol DID and anxiety. These findings suggest that HDID selection has not produced systematic changes in anxiety-like behavior or sensitivity to alcohol-induced anxiolysis, though there is a tendency in the male mice of the first replicate toward reduced basal anxiety-like behavior. Therefore, anxiety state and sensitivity to alcohol's anxiolytic effects do not appear to contribute significantly to the high drinking behavior of the HDID mice. Copyright © 2014 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 11/2014; DOI:10.1016/j.alcohol.2014.07.022
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    ABSTRACT: Maternal ethanol consumption during pregnancy can produce a range of teratogenic outcomes in offspring. The mechanism of ethanol teratogenicity is multi-faceted, but may involve alterations in insulin and insulin-like growth factor (IGF) signaling pathways. These pathways are not only important for metabolism, but are also critically involved in neuronal survival and plasticity, and they can be altered by chronic prenatal ethanol exposure (CPEE). The objective of this study was to test the hypothesis that CPEE alters expression of insulin and IGF signaling molecules in the prefrontal cortex and liver of adult guinea pig offspring. Pregnant Dunkin-Hartley-strain guinea pigs received ethanol (4 g/kg maternal body weight/day) or isocaloric-sucrose/pair-feeding (nutritional control) throughout gestation. Fasting blood glucose concentration was measured in male and female offspring at postnatal day 150–200, followed by euthanasia, collection of prefrontal cortex and liver, and RNA extraction. IGF-1, IGF-1 receptor (IGF-1R), IGF-2, IGF-2 receptor (IGF-2R), insulin receptor substrate (IRS)-1, IRS-2, and insulin receptor (INSR) mRNA expression levels were measured in tissues using quantitative real-time PCR. The mean maternal blood ethanol concentration was 281 ± 15 mg/dL at 1 h after the second divided dose of ethanol on GD 57. CPEE resulted in increased liver weight in adult offspring, but produced no difference in fasting blood glucose concentration compared with nutritional control. In the liver, CPEE decreased mRNA expression of IGF-1, IGF-1R, and IGF-2, and increased IRS-2 mRNA expression in male offspring only compared with nutritional control. Female CPEE offspring had decreased INSR hepatic mRNA expression compared with male CPEE offspring. In the prefrontal cortex, IRS-2 mRNA expression was increased in CPEE offspring compared with nutritional control. The data demonstrate that CPEE alters both central and peripheral expression of insulin and IGF signaling molecules at the mRNA level, which may be related to metabolic dysregulation in adult offspring. Furthermore, altered insulin and IGF signaling may be a mechanism of ethanol neurobehavioral teratogenicity.
    Alcohol (Fayetteville, N.Y.) 09/2014; DOI:10.1016/j.alcohol.2014.09.001
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    ABSTRACT: Alcohol increases the risk of injuring oneself and others. However, following an injury there appears to be a benefit to alcohol in mediating the body's response to a traumatic injury and reducing mortality. The physiological mechanism underlying this reported association is poorly understood. One approach to explaining the pathways by which alcohol affects acute mortality following a traumatic injury is to identify differential prevalence of medical complications associated with increased mortality. The goal of this study was to evaluate the association between blood alcohol concentration and complications subsequent to a traumatic injury that are associated with increased in-hospital mortality. This study involved a retrospective analysis of traumatic injuries occurring between 2000 and 2009 as reported by all level I and II trauma units in the state of Illinois. The study includes all patients with blood alcohol toxicological examination levels ranging from zero to 500 mg/dL and meeting additional inclusion criteria (n = 84,974). A reduction in complications of cardiac and renal function by 23.5% and 30.0%, respectively, was attributable to blood alcohol concentration. In addition, blood alcohol concentration was associated with fewer cases of pneumothorax and convulsions. However, blood alcohol concentration continued to be positively associated with aspiration pneumonitis and acute pancreatitis in the final models. The net impact of alcohol following an injury is protective, largely attributable to a reduction in complications relating to cardiac and renal function. This study helps to explain the observed protective effect from blood alcohol concentrations in reducing in-hospital mortality after an injury, as reported in many studies.
    Alcohol (Fayetteville, N.Y.) 06/2014; 48(4):391-400. DOI:10.1016/j.alcohol.2014.01.008
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    ABSTRACT: Sardinian alcohol-preferring (sP) rats have been selectively bred for high alcohol preference and consumption. When exposed to the standard, home cage 2-bottle “alcohol (10%, v/v) vs. water” choice regimen with continuous access, male sP rats consume daily approximately 6 g/kg alcohol. Conversely, when exposed to the intermittent (once every other day) access to 2 bottles containing alcohol (20%, v/v) and water, respectively, male sP rats display marked increases in daily alcohol intake and signs of alcohol intoxication and “behavioral” dependence. The present study was designed to assess alcohol intake in female sP rats exposed, under the 2-bottle choice regimen, to (a) 10% (v/v) alcohol with continuous access (CA10%), (b) 10% (v/v) alcohol with intermittent access (IA10%), (c) 20% (v/v) alcohol with continuous access (CA20%), and (d) 20% (v/v) alcohol with intermittent access (IA20%). Male sP rats (exposed to CA10% and IA20% conditions) were included for comparison. Over 20 daily drinking sessions, daily alcohol intake in female CA10% and IA20% rats averaged 7.0 and 9.6 g/kg, respectively. The rank of alcohol intake was IA20% > IA10% = CA20% > CA10%. Conversely, daily alcohol intake in male CA10% and IA20% rats averaged 6.0 and 8.2 g/kg, respectively. Comparison of female and male rats yielded the following rank of alcohol intake: female IA20% > male IA20% > female CA10% ≥ male CA10%. An additional experiment found that alcohol drinking during the first hour of the drinking session produced mean blood alcohol levels of 35–40 mg% and 85–100 mg% in the CA10% and IA20% rats, respectively. These results (a) extend to female sP rats previous data demonstrating the capacity of the IA20% condition to markedly escalate alcohol drinking, and (b) demonstrate that female sP rats consume more alcohol than male sP rats. This sex difference is more evident under the IA20% condition, suggesting that female sP rats are highly sensitive to the promoting effect of the IA20% condition on alcohol drinking. These data contribute to the characterization of sP rats as a model of excessive alcohol consumption.
    Alcohol (Fayetteville, N.Y.) 06/2014; DOI:10.1016/j.alcohol.2014.01.001
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    ABSTRACT: Instrumental behavior can shift from flexible, goal-directed actions to automatic, stimulus-response actions. The satiety-specific devaluation test assesses behavioral flexibility by evaluating reward seeking after temporary devaluation of the reinforcer via satiety; a decrease in responding compared to control conditions indicates goal-directed behavior. We have observed variability in the outcome of this test that may be dependent on the reinforcer. Another test of habit, contingency degradation, involves changing the action-outcome association over the course of retraining and determines whether reward seeking is sensitive to changing contingencies. We hypothesized that the outcome of the contingency-degradation test would remain consistent across reinforcers, while the satiety-specific devaluation test may vary across reinforcers because it depends on the ability of the reinforcer to induce satiety. Therefore, we trained rats to self-administer 1.5% sucrose, 10% sucrose, 10% ethanol, or 10 mm monosodium glutamate (MSG) on a fixed-ratio (FR5) schedule that has been shown to promote long-term, goal-directed responding. Next, behavioral flexibility was evaluated in three satiety-specific devaluation tests over 6 weeks. Finally, we investigated reward seeking after contingency-degradation training. All groups displayed sensitivity to satiety-specific devaluation in the first test, indicating goal-directed behavior. While the 10% sucrose and ethanol groups remained goal-directed, the 1.5% sucrose and MSG groups exhibited habit-like behavior in later tests. Nevertheless, all groups displayed decreased responding in an extinction session after contingency-degradation training, indicating goal-directed behavior. These results demonstrate that tests of behavioral flexibility can yield dissimilar results in the same rats. Next, rats from the 1.5% sucrose group underwent the entire experiment again, now self-administering 10% sucrose. These rats showed pronounced goal-directed behavior in satiety-specific and contingency-degradation tests under 10% sucrose conditions, further suggesting that the reinforcer solution affected the outcome of the satiety-specific devaluation test. We conclude that reinforcer characteristics should be considered when investigating habit-like behavior in alcohol research.
    Alcohol (Fayetteville, N.Y.) 06/2014; DOI:10.1016/j.alcohol.2013.12.006
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    ABSTRACT: It has become clear that adolescence is a period of distinct responsiveness to the acute effects of ethanol on learning and other cognitive functions. However, the effects of repeated intermittent ethanol exposure during adolescence on learning and cognition are less well studied, and other effects of repeated ethanol exposure such as withdrawal and chronic tolerance complicate such experiments. Moreover, few studies have compared the effects of repeated ethanol exposure during adolescence and adulthood, and they have yielded mixed outcomes that may be related to methodological differences and/or secondary effects of ethanol on behavioral performance. One emerging question is whether relatively brief intermittent ethanol exposure (i.e., sub-chronic exposure) during adolescence or adulthood might alter learning at a time after exposure when chronic tolerance would be expected, and whether tolerance to the cognitive effects of ethanol might influence the effect of ethanol on learning at that time. To address this, male adolescent and adult rats were pre-treated with sub-chronic daily ethanol (five doses [4.0 g/kg, i.p.] or saline at 24-h intervals, across 5 days). Two days after the last pre-exposure, spatial learning was assessed on 4 consecutive days using the Morris water maze. Half of the animals from each treatment cell received ethanol (2.0 g/kg, i.p.) 30 min prior to each testing session and half of the animals received saline. Ethanol pre-exposure altered water maze performance in adolescent animals but not in adults, and acute ethanol exposure impaired learning in animals of both ages independent of pre-exposure condition. There was no evidence of cognitive tolerance in animals of either age group. These results indicate that a relatively short period of intermittent ethanol exposure during adolescence, but not adulthood, alters baseline water maze performance shortly after pre-exposure and does not induce cognitive tolerance to the effects of ethanol in either age group.
    Alcohol (Fayetteville, N.Y.) 06/2014; DOI:10.1016/j.alcohol.2014.02.003
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    ABSTRACT: Ethanol induces appetitive, aversive, and anxiolytic effects that are involved in the development of ethanol use and dependence. Because early ethanol exposure produces later increased responsiveness to ethanol, considerable effort has been devoted to analysis of ethanol’s appetitive and aversive properties during early ontogeny. Yet, there is a relative scarcity of research related to the anxiolytic effects of ethanol during early infancy, perhaps explained by a lack of age-appropriate tests. The main aim of this study was to validate a model for the assessment of ethanol’s anxiolytic effects in the infant rat (postnatal days 13–16). The potentially anxiolytic effects of ethanol tested included: i) amelioration of conditioned place aversion, ii) ethanol intake in the presence of an aversive conditioned stimulus, iii) the inhibitory behavioral effect in an anxiogenic environment, and iv) innate aversion to a brightly illuminated area in a modified light/dark paradigm. Ethanol doses employed across experiments were 0.0, 0.5, and 2.0 g/kg. Results indicated that a low ethanol dose (0.5 g/kg) was effective in attenuating expression of a conditioned aversion. Ethanol intake, however, was unaffected by simultaneous exposure to an aversive stimulus. An anxiogenic environment diminished ethanol-induced locomotor stimulation. Finally, animals given 0.5 g/kg ethanol and evaluated in a light/dark box showed increased time spent in the illuminated area and increased latency to escape from the brightly lit compartment than rats treated with a higher dose of ethanol or vehicle. These new results suggest that ethanol doses as low as 0.5 g/kg are effective in ameliorating an aversive and/or anxiogenic state in preweanling rats. These behavioral preparations can be used to assess ethanol's anxiolytic properties during early development.
    Alcohol (Fayetteville, N.Y.) 06/2014; DOI:10.1016/j.alcohol.2014.01.007