Moderate Dose Of Alcohol Research Articles

Alcohol effects on inhibitory control of attention: distinguishing between intentional and automatic mechanisms

Recent research has begun to explore the possibility that inhibitory mechanisms of selective attention are particularly susceptible to the impairing effects of moderate doses of alcohol. However, literature also suggests that automatic processes might be more resistant to this impairing effect than controlled processes. The present study used a delayed ocular response task and a saccadic interference task to examine the effects of alcohol on both intentionally controlled and automatic inhibitory influences on selective attention. Twelve healthy adults performed both tasks under three doses of alcohol (0.0, 0.45, and 0.65 g/kg). The results showed that alcohol reduced intentional inhibitory control over selective attention but had no effect on automatic inhibitory influences. The present investigation marks the first effort to directly compare alcohol effects on automatic and intentional inhibitory mechanisms of visual attention. The results suggest that attentional processes dependent on intentional inhibitory control may be more susceptible to the impairing effects of a moderate dose of alcohol than processes dependent on automatic inhibition.

Rape-Myth Congruent Beliefs in Women Resulting from Exposure to Violent Pornography

Previous research findings indicate that women suffer a variety of detrimental effects from exposure to violent pornography. This study used an experimental paradigm to examine the effects of a moderate alcohol dose and alcohol expectancies on women's acute reactions to a violent pornographic stimulus. A community sample of female social drinkers (N = 134) read an eroticized rape depiction after completing an alcohol administration protocol. As predicted, intoxicated participants were less likely to label the depicted events as rape than their sober counterparts. A path analytic model illustrated that participants' self-reported sexual arousal to the stimulus, as influenced by alcohol consumption and expectancies, resulted in increased rape myth congruent perceptions of the victim and decreased labeling of the incident as rape. Findings suggest that acute alcohol intoxication during violent pornography exposure may ultimately result in women developing more calloused attitudes toward rape and rape victims.

Alcohol Attenuates Load‐related Activation During a Working Memory Task: Relation to Level of Response to Alcohol

A low level of response to alcohol is a major risk factor for the development of alcohol dependence, but neural correlates of this marker are unclear. Ten healthy volunteers were classified by median split on level of response to alcohol and underwent 2 sessions of functional magnetic resonance imaging following ingestion of a moderate dose of alcohol and a placebo. The blood oxygen level-dependent activation to an event-related visual working memory test was examined. The subjects exhibited longer response latencies and more errors as a function of increasing working memory load and showed a load-dependent increase in activation in dorsolateral prefrontal cortex, posterior parietal cortex, and visual cortex. Alcohol did not affect performance (errors or response latency), but attenuated the working memory load-dependent activation in the dorsolateral prefrontal cortex. During the placebo condition, individuals with a low level of response to alcohol showed greater activation in dorsolateral prefrontal cortex and posterior parietal cortex than those with a high level of response to alcohol. During the alcohol condition, groups showed similar attenuation of load-dependent brain activation in these regions. Low-level responders relative to high-level responders exhibited an increased working memory load-dependent activation in dorsolateral prefrontal cortex and posterior parietal cortex when not exposed to alcohol. This increase in brain response was attenuated in low-level responders after ingesting a moderate dose of alcohol.

Dopamine and Benzodiazepine-Dependent Mechanisms Regulate the EtOH-Enhanced Locomotor Stimulation in the GABAA α1 Subunit Null Mutant Mice

The present study investigated the role of the alpha1-containing GABA(A) receptors in the neurobehavioral actions of alcohol. In Experiment 1, mice lacking the alpha1 subunit (alpha1 (-/-)) were tested for their capacity to initiate operant-lever press responding for alcohol or sucrose. Alcohol intake in the home cage was also measured. In Experiment 2, the alpha1 (-/-) mice were injected with a range of alcohol doses (0.875-4.0 g/kg; i.p.) to evaluate the significance of the alpha1 subunit in alcohol's stimulant actions. In Experiment 3, we determined if the alcohol-induced stimulant effects were regulated via dopaminergic (DA) or benzodiazepine (BDZ)-dependent mechanisms. To accomplish this, we investigated the capacity of DA (eticlopride, SCH 23390) and BDZ (flumazenil, betaCCt) receptor antagonists to attenuate the alcohol-induced stimulant actions. Compared with wild-type mice (alpha1 (+/+)), the null mutants showed marked reductions in both EtOH and sucrose-maintained responding, and home-cage alcohol drinking. The null mutants also showed significant increases in locomotor behaviors after injections of low-moderate alcohol doses (1.75-3.0 g/kg). betaCCt, flumazenil, eticlopride, and SCH 23390 were able to attenuate the alcohol-induced stimulation in mutant mice, in the absence of intrinsic effects. These data suggest the alpha1 receptor plays an important role in alcohol-motivated behaviors; however, it also appears crucial in regulating the reinforcing properties associated with normal ingestive behaviors. Deleting the alpha1 subunit of the GABA(A) receptor appears to unmask alcohol's stimulatory effects; these effects appear to be regulated via an interaction of both DA- and GABA(A) BDZ-dependent mechanisms.

Effects of Alcohol on Sleep and the Sleep Electroencephalogram in Healthy Young Women

Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women. Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5- or 9-hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22-25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine. Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2-hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the alpha range (9-11 Hz) during all-night non-REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2-hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the alpha range in anterior derivations and within the delta range (3-4 Hz) in posterior derivations during the initial part of the night. A moderate dose of alcohol just before bedtime resulted in a short-lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep.

Alcohol consumption impairs stimulus- and error-related processing during a Go/No-Go Task

Alcohol consumption has been shown to increase the number of errors in tasks that require a high degree of cognitive control, such as a go/no-go task. The alcohol-related decline in performance may be related to difficulties in maintaining attention on the task at hand and/or deficits in inhibiting a prepotent response. To test these two accounts, we investigated the effects of alcohol on stimulus- and response-locked evoked potentials recorded during a go/no-go task that involved the withholding of key presses to rare targets. All participants performed the task prior to drinking and were then assigned randomly to either a control, low-dose, or moderate-dose treatment. Both doses of alcohol increased the number of errors relative to alcohol-free performance. Success in withholding a prepotent response was associated with an early-enhanced stimulus-locked negativity at inferior parietal sites, which was delayed when participants failed to inhibit the motor command. Moreover, low and moderate doses of alcohol reduced N170 and P3 amplitudes during go, no-go, and error trials. In comparison with the correct responses, errors generated large response-locked negative (Ne) and positive (Pe) waves at central sites. Both doses of alcohol reduced the Ne amplitude whereas the Pe amplitude decreased only after moderate doses of alcohol. These results are consistent with the interpretation that behavioral disinhibition following alcohol consumption involved alcohol-induced deficits in maintaining and allocating attention thereby affecting the processing of incoming stimuli and the recognition that an errant response has been made.

A Microdialysis Profile of Met-Enkephalin Release in the Rat Nucleus Accumbens Following Alcohol Administration

Pharmacological studies have implicated the endogenous opioid system in mediating alcohol intake. Other evidence has shown that alcohol administration can influence opioid activity. In this regard, the majority of studies have concentrated on endorphinergic systems, whereas other opioid systems have been granted comparably less attention. This is the case despite some compelling evidence that has implicated enkephalinergic peptide systems, particularly Met-enkephalin, in mediating alcohol preference. The aim of the present study was to investigate the effect of alcohol administration on extracellular levels of Met-enkephalin in the rat nucleus accumbens--a brain region that plays a significant role in the processes underlying reinforcement and stress. Male Sprague-Dawley rats were implanted with a microdialysis probe aimed at the shell region of the nucleus accumbens. Artificial cerebrospinal fluid was pumped at a rate of 1.75 mul/min in awake and freely moving rats and dialysates were collected at 30-minute intervals. After several baseline collections, rats were injected intraperitoneally with either physiological saline or one of four doses of alcohol: 0.8, 1.6, 2.4, or 3.2 g/kg ethanol body weight. The levels of Met-enkephalin in the dialysates were analyzed with solid-phase radioimmunoassay. Within the first 30 minutes of administration, an alcohol dose of 1.6 g/kg caused a significant and prolonged elevation in the extracellular levels of Met-enkephalin. Alcohol did not have a major effect on the release of Met-enkephalin at any other dose. In this experiment, only a moderate dose of alcohol was capable of stimulating Met-enkephalin release in the nucleus accumbens. Enkephalins may modulate local neurotransmitter release by binding to presynaptic Delta-opioid receptors, or, they may inhibit effector cells by binding to postsynaptic Delta- or mu-opioid receptors. This may be one of multiple neurological mechanisms that modulate alcohol-drinking behavior.

Acute tolerance to alcohol effects on inhibitory and activational mechanisms of behavioral control.

Acute alcohol tolerance refers to the observation of reduced impairment at a given blood alcohol concentration (BAC) on the descending versus ascending limb of the blood alcohol curve. Psychomotor performance measures used in human studies of alcohol tolerance provide reliable assessments of tolerance but do not identify specific mechanisms involved in the re-establishment of control, and little is known about how acute tolerance is expressed in terms of changes in fundamental mechanisms that regulate and control behavior. This study examined the expression of acute alcohol tolerance to impaired behavioral control in terms of changes in a drinker's ability to activate and inhibit behavioral responses as BAC ascended and declined following a dose. Twenty social drinkers performed a cued go/no-go task that measured behavioral control after receiving a moderate dose (0.65 g/kg) of alcohol and a placebo. The development of acute tolerance was measured by testing behavioral control twice: once during the ascending phase and again at comparable BACs during the descending phase of the blood alcohol curve. Inhibitory and activational aspects of behavioral control both were impaired by alcohol. Acute tolerance developed to the impaired activation but not to the impaired inhibition of behavior. The results highlight the importance of considering behavioral requirements when testing for the development of acute tolerance under a dose of alcohol. By modeling behavioral control as the net effect of countervailing activational and inhibitory influences, the study suggests that fundamental mechanisms of control might not display uniform tolerance development.

Moderate-Level Prenatal Alcohol Exposure Alters Striatal Dopamine System Function in Rhesus Monkeys

Moderate prenatal alcohol exposure can cause impairments even in the absence of gross morphological defects associated with fetal alcohol syndrome. The basal ganglia, which include the dopamine-rich striatum, are sensitive to fetal alcohol-induced injury. In this study, we manipulated the timing of moderate-level alcohol exposure and compared the risk of adverse effects on striatal dopamine (DA) system function in rhesus monkeys. Thirty-five young adult rhesus monkeys (Macaca mulatta) from four groups of females were assessed: (1) an early alcohol-exposed group (n=9), in which mothers voluntarily consumed 0.6 g/kg alcohol solution on gestational days 0 through 50; (2) a middle-to-late gestation alcohol-exposed group (n=7), in which mothers voluntarily consumed 0.6 g/kg alcohol solution on gestational days 50 through 135; (3) a continuous-exposure group (n=9), in which mothers voluntarily consumed 0.6 g/kg alcohol solution on days 0 through 135; and (4) controls (n=10), in which mothers voluntarily consumed an isocaloric control solution on gestational days 0 through 50, 50 through 135, or 0 through 135. We studied striatal DA system function by positron emission tomography in separate scans for trapping of [(18)F]fallypride and 6-[(18)F]fluoro-m-tyrosine to assess striatal DA D2 receptor (D2R) binding and DA synthesis, respectively, via dopadecarboxylase activity. Moderate-level alcohol exposure during early gestation and continuous exposure throughout gestation (early + middle-to-late exposure) reduced the striatal D2R binding to DA synthesis ratio, whereas middle-to-late alcohol gestation exposure increased the striatal D2R binding to DA synthesis ratio. The continuous-exposure group showed the largest effect. Moreover, the D2R binding/DA synthesis ratio was related to neonatal neurobehavior measures in control monkeys, but these relationships were disrupted in the fetal alcohol-exposed monkeys. These results suggest that the vulnerability of the DA system to the effects of moderate doses of alcohol during gestation depend on the timing of the alcohol exposure. Early-gestation moderate alcohol exposure resulted in a reduction or blunting of dopaminergic function in adulthood, whereas middle to late exposure (without early exposure) either induced the opposite pattern or heightened dopaminergic function. Continuously exposed monkeys showed the largest effect, suggesting that the sooner women stop drinking, the better it is for the fetus.

The effects of alcohol on cigarette craving in heavy smokers and tobacco chippers.

The authors examined the effects of alcohol consumption on cigarette craving in heavy smokers and tobacco chippers (n = 138) who were instructed not to smoke for 12 hr. Participants were exposed to both smoking cues (a lit cigarette) and control cues. Half received a moderate dose of alcohol, adjusted for gender, and half received a placebo. Results indicated that alcohol consumption produced an increase in urge-to-smoke ratings before smoking cue exposure. Moreover, during cue exposure, alcohol consumption produced a sharper increase in urge ratings than did the placebo. In addition, during smoking cue exposure, alcohol increased the likelihood of displaying facial expressions associated with positive affect. These findings suggest that alcohol consumption influences both the magnitude and the emotional valence of cigarette cravings.

Selective GABAA ??5 Benzodiazepine Inverse Agonist Antagonizes the Neurobehavioral Actions of Alcohol

Previous research has implicated the alpha5-containing GABAA receptors of the hippocampus in the reinforcing properties of alcohol. In the present study, a selective GABAA alpha5 benzodiazepine inverse agonist (e.g., RY 023) was used in a series of in vivo and in vitro studies to determine the significance of the alpha5-receptor in the neurobehavioral actions of alcohol. In experiment one, systemic injections of RY 023 (1 to 10 mg/kg IP) dose-dependently reduced ethanol-maintained responding by 52% to 86% of controls, whereas bilateral hippocampal infusions (0.3 to 20 microg) reduced responding by 66% to 84% of controls. Saccharin responding was reduced only with the highest intraperitoneal (e.g., 10 mg) and microinjected (e.g., 20 microg) doses. In experiment two, RY 023 (3.0 to 15 mg/kg IP) reversed the motor-impairing effects of a moderate dose of alcohol (0.75 g/kg) on an oscillating bar task in the absence of intrinsic effects. In the open field, RY 023 (3.0 to 7.5 mg/kg) produced intrinsic effects alone but attenuated the suppression of the 1.25 g/kg ethanol dose. Because the diazepam-insensitive receptors (e.g., alpha4 and alpha6) have been suggested to play a role in alcohol motor impairing and sedative actions, experiment three compared the efficacy of RY 023 with Ro 15-4513 and two prototypical benzodiazepine antagonists (e.g., flumazenil and ZK 93426) across the alpha4beta3gamma2-, alpha5beta3gamma2-, and alpha6beta3gamma2-receptor subtypes in Xenopus oocytes. RY 023 produced classic inverse agonism at all receptor subtypes, whereas Ro15-4513 and the two antagonists displayed a neutral or agonistic profile at the diazepam-insensitive receptors. Overall, the results extend our previous findings by demonstrating that an alpha5-subtype ligand is capable of attenuating not only the rewarding action of alcohol but also its motor impairing and sedative effects. We propose that these actions are mediated in part by the alpha5-receptors of the hippocampus. The hippocampal alpha5-receptors could represent novel targets in understanding the neuromechanisms regulating the neurobehavioral actions of alcohol in humans.

The acute effect of alcohol on decision making in social drinkers

Many studies have reported the long-term adverse effects of alcohol on executive cognitive function in chronic alcohol abusers, yet little research has investigated the acute effects of alcohol in social drinkers. Studies on acute effects report alcohol-induced deficits on tasks that require executive cognitive processes, with alcohol acting to increase preservative errors and reduce planning. The present investigation examines the acute effects of a moderate dose of alcohol on a decision-making task that involves participants making a forced choice between two simultaneously presented binary-outcome gambles. Alcohol (0.6 g/kg) or placebo was administered to 32 social drinkers. Participants completed the task, making a total of 80 decisions about gambles that varied in the magnitude of expected gains, losses and the probability with which these outcomes were delivered. Participants also chose between gambles probing identified non-normative biases in human decision making, namely, risk aversion for choosing between gains and risk seeking for choosing between losses. All participants picked the experimental gamble more frequently when the probability of winning was high vs low, when the gains were large vs small and when the losses were small vs large; the alcohol group had an impaired ability to factor in the magnitude of gains and the likelihood of winning when the losses were large. Deliberation time did not differ between the groups. These data suggest that alcohol given acutely impairs risky decision making. In particular, alcohol impairs one's ability to alter responding in light of changing prospective rewards in order to make favourable decisions.

Are bad drivers more impaired by alcohol?: Sober driving precision predicts impairment from alcohol in a simulated driving task

The contribution of driver experience to risk for alcohol-related crashes is based on the tacit assumption that driver experience contributes to driver skill which could mediate the impairing effects of alcohol on driving performance. Surprisingly, few studies of alcohol effects on simulated driving performance have examined the role of driver skill as a mediator of the intensity of alcohol impairment. The present study examined the degree to which individual differences in driving skill mediated the intensity of impairment produced by a moderate dose of alcohol in a group of young adult drivers. Twenty-eight participants were familiarized with a simulated driving road test. After determining their baseline skill level, participants’ driving performance was re-tested under either an active dose of alcohol (0.65 g/kg) or a placebo. Results showed that alcohol reduced driving precision, as evident by the increased within-lane deviation observed under the drug. Moreover, those individuals with poorer baseline skill levels showed the greater impairments in response to alcohol. The results highlight the importance of understanding interactions between driver skill level and the effects of alcohol and possibly other drugs.

Alcohol increases cognitive biases for smoking cues in smokers

Alcohol increases the motivation to smoke, possibly because it increases the incentive motivational properties of smoking cues. We examined whether alcohol would increase attentional, approach, and evaluative biases for smoking-related cues in a sample of daily cigarette smokers. The study used a visual probe task with eye movement recording to investigate biases in visual orienting to smoking-related cues. A stimulus-response compatibility task was used to assess approach tendencies for smoking-related cues, and an explicit rating task was used to assess the perceived valence of smoking-related cues. Participants completed the tasks in two sessions, once after consumption of 0.4 g/kg alcohol and once after consumption of a non-alcoholic drink. Alcohol increased the maintenance of attention on smoking cues (evident from gaze duration and a reaction time index of attentional bias), the perceived pleasantness of smoking cues, and cigarette craving, relative to the non-alcoholic drink. However, alcohol had no effect on the initial shifting of gaze to smoking cues or on the tendency to approach smoking cues. These results suggest that, in smokers, ingestion of a moderate dose of alcohol increases the propensity for smoking-related cues to hold attention and makes those cues seem more attractive, which is consistent with alcohol increasing the 'incentive salience' of smoking cues.

The level of response to alcohol in daughters of alcoholics and controls

Background: The low level of response (LR) to alcohol is a genetically influenced characteristic related to the development of alcohol use disorders (AUDs). This phenotype is found in men with a family history (FH) of alcoholism, predicts future AUDs, and has heritabilities as high as 60%. However, despite evidence of genetic influences for AUDs in both sexes, the majority of studies evaluating differences in LR across high- and low-risk groups have been conducted on males, and it is unclear how generalizable these results are to women. Methods: Twenty-five women who are family history positive (FHP) for alcohol dependence were matched with 25 women with no FH of alcoholism (FHN) on factors that may impact LR. Using an alcohol challenge paradigm, data on the reaction to a moderate dose of alcohol were gathered over a period of 3.5 h. Assessments included breath alcohol concentrations (BrACs), the Subjective High Assessment Scale (SHAS), as well as body sway or static ataxia. Results: Family history positives reported lower subjective intoxication than FHNs. In addition, when body sway scores were corrected for skewness, FHPs had significantly lower scores on alcohol-related changes in lateral sway. These differences remained after considering the effects of drinking history and BrAC values. Conclusions: This study evaluated the LR to alcohol in the largest sample of alcohol challenges in matched FHP and FHN women to date. Overall, the findings are consistent with most data from earlier investigations of smaller sized samples of FHP women. The results suggest that, similar to sons of alcoholics, a low LR to alcohol might also be characteristic of daughters of alcoholics.

Pleasure and alcohol: manipulating pleasantness and the acute effects of alcohol on food intake

To examine the effects of manipulating pleasantness on subsequent energy intake following a moderate dose of alcohol, 12 males attended the laboratory on four occasions. On each occasion participants consumed breakfast then 4 h later were offered lunch. Twenty minutes before lunch participants received an alcohol (24 g ethyl alcohol, 1508 kJ, 405 ml) or a no-alcohol (867 kJ, 405 ml) containing beverage followed by a lunch of either “bland” (rated pleasantness=66±13 mm) or “flavoured” (73±10 mm) foods. Subjective ratings of appetite, mood and pleasantness of several bland and tasty foods were taken before and after preloads and lunch. Ad libitum energy intake at lunch was greater following alcohol in both taste conditions ( p<0.01) (Alcohol/Bland, 2053±663 kJ; Alcohol/Flavoured, 1989±580 kJ) in comparison to the no-alcohol conditions (No-alcohol/Bland, 1548±357 kJ; No-alcohol/Flavoured 1670±401 kJ). No additive effect of palatability and alcohol was found; alcohol did not differentially affect intake of lunch items. Nor did alcohol increase the pleasantness of foods. Sensory specific satiety (SSS) was observed both following the preload and following lunch, with no discernible effects of alcohol on SSS. In conclusion, alcohol promoted food intake but this did not occur via the additive effects of alcohol and palatability nor through increasing the pleasantness of the taste of foods. Further research on the mechanism underlying the stimulating effects of alcohol on appetite is warranted.

Influence of Physical Attractiveness and Alcohol on Men's Perceptions of Potential Sexual Partners and Sexual Behavior Intentions.

The current research presents the results of 2 related experimental studies designed to evaluate the influence of physical attractiveness and a moderate dose of alcohol on men's perceptions of potential sexual partners and sexual behavior intentions. Analyses revealed significant effects of physical attractiveness on partner perceptions and sexual behavior intentions. Although no main effects of alcohol were observed, alcohol differentially moderated the relations between perceived risk and sexual behavior intentions by limb of absorption. Results suggest that greater attention should be focused on identifying the specific physical characteristics of a potential sexual partner--beyond attractiveness--that influence perceptions of risk and intentions to engage in safer sex behaviors and highlight the importance of assessing limb of absorption in evaluating the complex association between alcohol and risky sexual behavior.

Role of Alcohol Consumption in Escalation to Violence

No other drug has been associated with aggressive and violent behavior more than alcohol has. A major characteristic of the link between alcohol and social interactions is the very large variation in who becomes more aggressive while drinking and who does not. Tracing the origins of these individual differences has led to a focus on predispositions, such as the antisocial behavior of Type 2 alcoholics. Successful development of an experimental procedure to model heightened aggressive behavior after voluntary consumption of alcohol has facilitated the neurobiologic analysis of the link between alcohol and aggression. From a pharmacologic perspective, consumption of low to moderate doses of alcohol engenders heightened aggressive behavior in a significant minority of individuals before the circulation of appreciable amounts of the aldehyde metabolite. Ionophoric receptors such as NMDA, 5-HT(3) and GABA(A) have been identified in the brain as major sites of action for alcohol in the dose range that is relevant for engendering heightened aggression. Actions at the GABA(A) receptor complex that depend on particular GABA(A) subunits appear to be necessary for alcohol-heightened aggression. Genes that encode the synthesis of these alpha and gamma subunits are potentially significant markers for those individuals that are prone to engage in heightened aggressive behavior after the consumption of alcohol. Of particular importance are the reciprocal interactions between GABA and serotonin. Activating specific serotonin receptor subtypes such as 5-HT(1B) receptors reduces alcohol-heightened aggressive behavior. How these GABAergic and serotonergic corticolimbic mechanisms for alcohol-heightened aggression develop during the adolescent period remains an area of urgent study.

Gender differences in alcohol's disinhibiting effects: a commentary on Fillmore and Weafer.

Fillmore & Weafer (2004) present some very interesting and potentially important results suggesting that men are more susceptible than women to both the disinhibiting and stimulating effects of a moderate dose of alcohol. Research suggests that men are more susceptible than women to the disinhibiting effects of alcohol on aggression (Giancola & Zeichner 1995; Giancola et al. 2002), and, it has been well documented that men drink more and have more alcohol-related problems than women (Williams et al. 1989; Finn & Hall 2004). The present results suggest a potential mechanism that might contribute to these important gender differences. Alcohol may compromise inhibitory control of certain processes in men more than women, resulting in a tendency for men to consume more drinks on a single occasion than women, and a tendency for men to be more aggressive than women when intoxicated. Although the gender differences observed by Fillmore and Weafer make sense given the known gender differences in excessive alcohol use and alcohol-related problems, a number of questions need to be systematically addressed to establish the reliability of these effects. The first word of caution stems from the small sample size used in this study. Larger sample sizes are necessary to ensure that the observed gender differences are not just an oddity of the small sample. Furthermore, if these are true gender differences then it is important to assess whether they are reliable across time, dose level, blood alcohol concentration limb location, risk-status, and context. In fact, systematic study of the reliability and correlates of gender differences in the disinhibiting effects of alcohol would be helpful in uncovering the mechanisms responsible for this effect, if it is a true effect, and their relevance for broader gender differences in alcohol consumption and problems. If the differences are observed only at specific dosage levels or in specific contexts, then this might clarify some of the mechanisms underlying this effect. The authors discuss this issue to some degree when noting that gender differences in the disinhibiting effects of alcohol have not been observed on some inhibitory control tasks, such as the the stop-signal task (Mulvihill, Skilling & Vogel-Sprott 1997). We also have not observed gender differences in the disinhibiting effect of alcohol on a different go/no-go task that uses monetary incentives and punishments to activate or inhibit behavior (Finn et al. 1999). Gender differences also might vary in relation to risk status. For instance, while moderate drinking women appear to have significantly fewer alcohol problems than moderate drinking men, heavy drinking women appear to have equal or more alcohol-related problems than heavy-drinking men (Wilsnack, Wilsnack & Klassen 1984), suggesting that heavy drinking women may be more disinhibited than heavy-drinking men. Finally, the authors offer an interesting speculation that the gender differences in alcohol's stimulating effects may contribute to the observed differences in alcohol's disinhibiting effect. This is intuitively appealing speculation, but the authors can directly test this speculation by assessing whether alcohol-induced decreases in response inhibition are correlated with alcohol-induced increases in subjective stimulation. In summary, the gender differences in alcohol's disinhibiting effect observed by Fillmore and Weafer are potentially important and may have relevance for gender differences in alcohol consumption and problems. However, it is important to systematically study these effects in larger samples that vary in risk status while using different tasks, doses, and contexts. Such work will be very valuable to our understanding of broader gender differences in alcohol use and abuse and the mechanisms contributing to these differences.

Alcohol impairment of behavior in men and women.

Studies have shown that alcohol impairs the ability to inhibit behavioral responses in humans and some evidence suggests that men might display greater impairment than women. The present study compared men and women in the degree to which a moderate dose of alcohol impaired their inhibitory control at comparable blood alcohol concentrations. Twelve male and 12 female adult social drinkers received a moderate dose of alcohol (0.65 g/kg) and a placebo in a counterbalanced order and performed a cued go/no-go task that measured the ability to inhibit and execute behavioral responses. When the behavioral response was pre-potent (i.e. instigated), men displayed greater impairment of inhibitory control under alcohol than women. Men also reported greater levels of subjective stimulation from alcohol compared with women, who reported more sedation from the drug. A gender difference in alcohol impairment of inhibitory control could account for observations that disinhibited and aggressive behaviors under alcohol are more pronounced in men than in women.