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Ethanol has been demonstrated to exert profound effects upon cells and tissues via multiple mechanisms. One recently appreciated means by which cells can communicate with other cells is via the production and release of extracellular vesicles. Though smaller exosomes have been demonstrated to be released in response to ethanol exposure, the ability of ethanol to modulate the generation and release of larger microvesicle particles (MVP) is lesser studied. The present studies examined the ability of exogenous ethanol to generate MVP with a focus on skin cells. Acute ethanol exposure resulted in augmented MVP release in keratinocytes and in the skin and blood of mice. Unlike other stimuli such as ultraviolet B radiation or thermal burn injury, ethanol-mediated MVP release was independent of the Platelet-activating Factor receptor (PAFR). However, ethanol pretreatment was found to augment thermal burn injury-induced MVP in a PAFR-dependent manner. These studies provide a novel mechanism for ethanol-mediated effects, that could be relevant in the significant toxicity associated with thermal burn injury in the setting of alcohol intoxication.

The mean population age of the United States continues to increase, and data suggest that by the year 2060 the population of people over the age of 65 will more than double, providing a potentially massive strain on health care systems. Research demonstrates individuals 65 and older continue to consume ethanol, often at high levels. However, preclinical animal models are still being developed to understand how ethanol might interact with the aged population. The current experiments investigated differential body temperature responses in aged rats compared to adult rats and adolescent rats. Aged (19 months of age), adult (70 days of age), or adolescent (30 days of age) male Sprague Dawley rats were administered 1.0 g/kg, 2.0 g/kg, or 3.0 g/kg ethanol, intraperitoneally (i.p.), in a balanced Latin square design. Prior to ethanol administration, a core body temperature via an anal probe was obtained, and then repeatedly determined every 60 min following ethanol exposure for a total of 360 min. In addition, a blood sample was obtained from a tail nick 60, 180, and 300 min following the ethanol injection to investigate the relationship of ethanol levels and body temperature in the same animals. Aged rats had significantly greater reductions in body temperature compared to either adult or adolescent rats following both the 2.0 g/kg and 3.0 g/kg ethanol injection. Additionally, adolescent rats cleared ethanol significantly faster than aged or adult animals. These experiments suggest body temperature regulation in aged rats might be more sensitive to acute ethanol compared to adult rats or adolescent rats. Future studies are needed to identify the neurobiological effects underlying the differential sensitivity in aged rats to ethanol.

The present studies investigated the effects of withdrawal from a single binge-like dose of ethanol (hangover) on fear conditioning in male and female Sprague Dawley rats. In Experiment 1, males and females were given 0 or 3.5 g/kg ethanol intraperitoneally (i.p.) and then conditioned to contextual fear 24 h post injection. Withdrawal from acute ethanol enhanced expression of the conditioned freezing response in males, but not in females. Experiment 2 demonstrated that in males, withdrawal from acute ethanol administered 24 h prior to conditioning enhanced contextual fear conditioning, but not auditory-cued fear conditioning. In Experiment 3, male and female rats were given 3.5 g/kg ethanol, and blood ethanol concentrations (BECs) were assessed at various time points for determination of ethanol clearance. Female rats cleared ethanol at a higher rate than males, with 10 h required for females and 14 for males to eliminate ethanol from their systems. Because females cleared ethanol faster than males, in Experiment 4, females were conditioned 18 h after ethanol administration to keep the interval between ethanol clearance and fear conditioning similar to that of males. Withdrawal from acute ethanol given 18 h prior to conditioning did not affect both contextual and auditory-cued fear conditioning in females. In summary, these results highlight sex differences in the impact of withdrawal from acute ethanol (hangover) on fear learning; suggesting that males are more sensitive to hangover-associated enhancement of negative affect than females.

Taurine and alcohol has been popularly ingested through energy drinks. Reports from both compounds shows they are active on nervous system but little is known about the acute effect of these substances on the frontal cortex in an exercise approach. The aim of this study was to determine the effects of 0,6mldL-1 of ethanol (ET), 6g of taurine (TA), and taurine with ethanol (TA+ET) intake on absolute alpha power (AAP) in the frontal region, before and after exercise. Nine participants were recruited, five women (22±3years) and four men (26±5years), for a counterbalanced experimental design. For each treatment, the tests were performed considering three moments: "baseline", "peak" and "post-exercise". In the placebo treatment (PL), the frontal areas showed AAP decrease at the post-exercise. However, in the TA, AAP decreased at peak and increased at post-exercise. In the ET treatment, AAP increased at the peak moment for the left frontal electrodes. In the TA+ET treatment, an AAP increase was observed at peak, and it continued after exercise ended. These substances were able to produce electrocortical activity changes in the frontal regions after a short duration and low intensity exercise. Left and right regions showed different AAP dynamics during peak and post-exercise moments when treatments were compared.

Zebrafish is becoming a species of choice in neurobiological and behavioral studies of alcohol-related disorders. In these efforts, the activity of adult zebrafish is typically quantified using indirect activity measures that are either scored manually or identified automatically from the fish trajectory. The analysis of such activity measures has produced important insight into the effect of acute ethanol exposure on individual and social behavior of this vertebrate species. Here, we leverage a recently developed tracking algorithm that reconstructs fish body shape to investigate the effect of acute ethanol administration on zebrafish tail-beat motion in terms of amplitude and frequency. Our results demonstrate a significant effect of ethanol on the tail-beat amplitude as well as the tail-beat frequency, both of which were found to robustly decrease for high ethanol concentrations. Such a direct measurement of zebrafish motor functions is in agreement with evidence based on indirect activity measures, offering a complementary perspective in behavioral screening.

In human adolescents, sociable males frequently drink to enhance positive emotional states, whereas anxious females often drink to avoid negative affective states. This study used a rat model of adolescence to provide information regarding possible sex differences in contributors to social drinking. The effects of ethanol (0, 0.5, and 0.75g/kg) on play fighting and social preference were assessed on P30, P32, and P34 using a within-subject design. Then animals were tested in a social drinking paradigm (P37-P40), with this testing revealing high drinkers and low drinkers. Sex differences in sensitivity to ethanol emerged among high and low drinkers. High socially drinking males, but not females, when tested prior to drinking sessions, showed significant increases in play fighting at both doses. In low drinking males, play fighting was increased by 0.5g/kg ethanol, whereas the higher dose of 0.75g/kg produced significant decreases in play fighting. High drinking females initially showed low levels of social preference than high drinking males and low drinking females and were extremely sensitive to ethanol-induced enhancement of this social measure. Low social drinkers, both males and females, were more sensitive to the suppressing effects of ethanol on social preference following 0.75g/kg ethanol. These findings indicate that during adolescence enhanced sensitivity to the facilitating effects of ethanol on play fighting is associated with heavy drinking among males, whereas low social preference together with high sensitivity to ethanol-induced enhancement of social preference is related to high social drinking in females. Language: en

The zebrafish has been proposed for the study of the effects of ethanol on the vertebrate brain. Behavioural tests have been successfully employed in the phenotypical characterization of these effects. However, the short scale (minute to minute) time course of ethanol induced changes of zebrafish behaviour has not been analyzed. The current study alleviates this need using a 2 × 3 chronic × acute ethanol exposure experimental design. We first expose zebrafish to ethanol chronically using a dose escalation procedure in which fish are kept in a final concentration of 0.5% vol/vol ethanol for 10 days while control fish receive identical dosing procedures but no ethanol. Subsequently, we expose zebrafish for one hour to an acute dose of ethanol (0.00, 0.50, or 1.00 % vol.vol) and monitor their behaviour throughout this. period. We quantify the mean and within-individual temporal variance of distance travelled, distance from bottom and angular velocity using video-tracking, and establish temporal trajectories of ethanol induced behavioural changes in zebrafish. For example, we find fish of the highest acute dose group previously not exposed to chronic ethanol to exhibit an inverted U shaped temporal trajectory in distance travelled (biphasic alcohol effect). We find this response to be blunted after chronic ethanol exposure (development of tolerance). We also describe an acute ethanol withdrawal induced increase in angular velocity. We conclude that temporal analysis of zebrafish behaviour is a sensitive method for the study of chronic and acute ethanol exposure induced functional changes in the vertebrate brain.

Adolescents drink largely in social situations, likely in an attempt to facilitate social interactions. This study sought to examine alterations in the incentive salience of a social stimulus following repeated stress exposure and acute ethanol administration in adolescent and adult male Sprague–Dawley rats. Subjects were either exposed to 5 days of restraint stress, chronic variable stress (CVS), which consisted of a different stressor every day, or non-stressed. On test day, the animals were injected with 0, 0.25, 0.5, or 0.75 g/kg ethanol and placed in a social approach test in which they could see, hear, and smell a social conspecific, but could not physically interact with it. All the animals showed an interest in the social stimulus, with adolescents engaging in more social investigation than adults. Restraint stressed adults showed ethanol-induced increases in social investigation, while ethanol effects were not seen in any other group. An ethanol-associated increase in 50 kHz ultrasonic vocalization (USV) production was only evident in restraint stressed adolescents following 0.75 g/kg ethanol. 50 kHz USVs were not correlated with time spent investigating the social stimulus in any test condition. These results show that age differences in the facilitatory effects of ethanol on incentive salience of social stimuli are moderated by stress, with the facilitation of social approach by ethanol only evident in restraint stressed adults.

Ethanol has been suggested to have an anxiolytic effect on zebrafish, primarily based on its disruption of the novel tank diving response and of some social behaviors. The light/dark preference test offers a complementary measure of anxiety-like behavior in fish, and the purpose of the current study was to determine the effects of acute ethanol exposure on behavior in the light/dark task. In Experiment 1, the stimuli used to induce light/dark preference in zebrafish were varied in order to determine how best to measure the behavior. Subjects exhibited phototaxis (preference for light) when illumination was manipulated, but scototaxis (preference for dark) when wall and substrate color were manipulated. There was a clear interaction between locomotor activity and color preference, with animals preferentially freezing in darker locations. Because of ambiguity in interpreting behavior in the open/covered version of the test, the black/white version was used in Experiment 2. In Experiment 2, zebrafish were exposed to ethanol (0.25%, 0.5%, or 1.0%) or water for 30 minutes, and then placed in a black/white preference tank containing either ethanol (same doses) or water for a 30-minute test. Ethanol exposure increased locomotor activity and reduced freezing. Additionally, there was a significant interaction between ethanol treatment and locomotor activity on side preference. Low doses of ethanol increased white avoidance in normally swimming fish, while high doses did not.

Gender-related differential sensitivity to ethanol has long been recognized. Our previous studies have demonstrated that the zebrafish, an animal model used currently to study genetics and development related to a variety of human diseases, is also sensitive to pharmacologically relevant concentrations of ethanol. Sensitivity to ethanol in the zebrafish can be easily gauged with a simple nonintrusive behavioral test that measures ethanol-related alterations in schooling by determining the distance between each fish and its nearest neighbor. The purpose of this study was to determine the influence of gender on the strain-specific ethanol sensitivity that we had observed previously. One hundred and sixty zebrafish of the wild-type (WT) and the long fin striped (LFS) strains were equally divided by gender for use in this study. For acute ethanol treatment, the fish were separated by gender and strain and exposed to 0.0, 0.125, 0.25 0.50, or 1.0% (vol/vol) ethanol. In the chronic study, eight fish of each strain and gender were exposed to 0.5% (vol/vol) ethanol for a period of 10 weeks and the swimming behavior tested before treatment and after each week of treatment. Results showed that female WT zebrafish displayed enhanced sensitivity to the effects of chronic ethanol exposure of increased nearest neighbor distances, whereas male and female LFS fish were not significantly affected by chronic ethanol exposure. Results of the acute ethanol study showed a dose-dependent effect in both strains and a gender effect that needs to be further investigated before enhanced female sensitivity to acute ethanol can be verified.

Acetaldehyde, salsolinol (Sal), and 6-hydroxy-1-methyl-1,2,3,4-tetrahydro-β-carboline (6-OH-MTHβC) in neonatal rat brain after acute ethanol treatment were determined by high performance liquid chromatography (HPLC). Free acetaldehyde in rat brain homogenate was derivatized with 2,4-dinitrophenylhydrazine at 60°C for 15 min. The derivatized product was separated on an octadecylsilane-C18 column (150 mm×4.6 mm, 5 μm) and detected with HPLC at 360 nm. The method was proved to be simple, sensitive, and reliable. Compared with control, analysis of neonatal rat brain samples revealed a significant difference in the level of acetaldehyde within 24 h of 5.0 g/kg ethanol treatment (P < 0.05). Also the level of Sal and 6-OH-MTHβC was determined by HPLC performed on a HS F5 column (250 mm×4.6 mm, 5 μm), using Coularray Detector-4 as the electrochemical detector. The results indicated that the levels of Sal and 6-OH-MTHβC in rat brain increased significantly with the elevated level of acetaldehyde after acute alcohol administration. The condensation of acetaldehyde with monoamine neurotransmitters after alcoholism may play an important role in central nervous system dysfunction.

Recent findings suggest that the ability of ethanol (EtOH) to increase the levels of neurosteroids with potent γ-aminobutyric acid (GABA)ergic properties can influence measures of EtOH sensitivity. Earlier studies determined that removal of the adrenals and gonads diminished the steroidogenic effect of EtOH and significantly increased acute EtOH withdrawal severity in two inbred mouse strains that differed in withdrawal severity, suggesting the contribution of anticonvulsant GABAergic steroids to acute withdrawal in intact animals. Thus, the goal of the present studies was to investigate the consequence of steroid removal on acute EtOH withdrawal through excision of the adrenals and gonads, in another genetic animal model of EtOH withdrawal differences, the Withdrawal Seizure-Prone (WSP) and -Resistant (WSR) selected lines. Male and female WSP and WSR mice underwent surgical removal of the adrenals and gonads or no organ removal (SHAM). One to two weeks later, baseline handling-induced convulsions (HICs) were assessed, mice were given a 4 g/kg dose of ethanol, and HICs were measured hourly for 12 hours and then at 24 hours. The combination surgery significantly increased EtOH withdrawal in WSP and WSR female mice, as measured by area under the curve (AUC) and peak HIC scores. AUC was significantly positively correlated with plasma corticosterone levels and significantly negatively correlated with progesterone levels. In contrast, surgical status did not alter withdrawal severity in male WSP and WSR mice. Overall, the increase in acute ethanol withdrawal severity in female WSP and WSR mice following adrenalectomy and gonadectomy corroborate our recent evidence that withdrawal from a high dose of EtOH can be modulated by anticonvulsant steroids produced in the periphery.

We previously reported significant sex differences in ethanol withdrawal (EW) recovery as well as in sensitivity to GABAA receptor modulators during EW. The aim of the present study was to determine if hormonal status moderated behavioral responses to an acute ethanol challenge in EW animals comparing two different behaviors. An initial set of experiments explored motor-incoordinating effects of the acute ethanol injection during EW at either 1 day or 3 days of withdrawal. EW male, but not female, rats showed a decrease in coordination compared to controls that persisted through 3 days EW. Female rats displayed tolerance to the motor-incoordinating actions of the acute ethanol challenge at 1 day EW whereas tolerance was more evident in EW male rats at 3 days. In contrast, EW animals generally remained responsive to the anticonvulsant actions of ethanol, irrespective of hormonal status. While EW by itself did not significantly alter seizure latency, duration or severity, it increased seizure-induced mortality especially at 3 days EW. There was some evidence of tolerance to the anticonvulsant effect of the acute ethanol challenge at the lowest dose employed (0.62 g/kg), which varied by sex condition and time of EW. All sex conditions displayed marked sensitivity to the anticonvulsant effects of the ethanol challenge at the two higher doses studied. Overall, ovariectomized females showed the greatest response to the acute ethanol administration. These findings provide additional evidence of a divergence in behavioral responses during EW and suggest that multiple neuroadaptations moderate various responses to ethanol during EW, with minor contributions of hormonal status.

The zebrafish has been a popular subject of embryology and genetic research for the past three decades. Recently, however, the interest in its neurobiology and behavior has also increased. Nevertheless, compared to other model organisms, e.g., rodents, zebrafish behavior is understudied and very few behavioral paradigms exist for mutation or drug screening purposes. Alcoholism is one of the biggest and costliest diseases whose mechanisms are not well understood. Model organisms such as the zebrafish may be utilized in this line of research. Previously, we investigated the effects of acute ethanol exposure on adult zebrafish using four behavioral paradigms and employing manual quantification methods. Here, we study the effects of chronic ethanol exposure and analyze how it modifies the effects of acute ethanol treatment. We employ a videotracking-based automated quantification method in a predator model paradigm and show that this method is capable of detecting an avoidance reaction that is ameliorated by higher doses of ethanol, a potential anxiolytic effect. Importantly, we also demonstrate that chronic, two week long, exposure to ethanol results in significant adaptation to this substance in adult zebrafish. Overall, our results suggest that zebrafish will be an appropriate subject for high throughput screening applications aimed at the analysis of the mechanisms and pharmacology of acute and chronic ethanol induced changes in the vertebrate brain.

Withdrawal from an acute bolus injection of ethanol produces affective or emotional signs that include anxiogenic-like behavior (Gauvin et al., 1992) and conditioned place aversion (Morse et al., 2000). The current study assessed whether brain reward deficits that accompany withdrawal from chronic ethanol dependence (Schulteis et al., 1995) are also observed upon withdrawal from acute intoxication. Rats were implanted with stimulating electrodes aimed at the medial forebrain bundle in the lateral hypothalamus and trained on a discrete trial current-intensity brain stimulation reward threshold paradigm. Ethanol intoxication was produced by bolus intraperitoneal injections of ethanol (1.0, 1.5, or 2.0 g/kg). Brain reward thresholds were monitored periodically following the bolus injection (3, 6, 9, 12, 24, 48, 72, 96 hr post-ethanol). Blood samples taken at various intervals post-ethanol revealed that peak blood alcohol levels (BAL) at all doses tested were reached within 10 min of injection. Following doses of 1.0, 1.5 and 2.0 g/kg ethanol, BAL had declined to undetectable levels within 3–6 hr post-injection. Withdrawal from a single injection of ethanol resulted in a significant but transient increase in brain reward thresholds only with the highest ethanol dose tested (2.0 g/kg). When acute intoxication and withdrawal episodes were repeated two additional times at weekly intervals, the peak magnitude and duration of threshold elevation increased significantly at the 2.0 g/kg dose of ethanol. A significant but transient increase in thresholds was also seen in the group treated with 1.5 g/kg ethanol during the 3rd and final week of testing. Results indicate that withdrawal from a single exposure to an intoxicating dose of ethanol produces significant brain reward deficits in addition to other affective disturbances previously reported, and that repeated weekly intoxication and withdrawal results in a progressive increase in magnitude and duration of the reward deficit.

Rodents are particularly prone to acquire associative memories during early stages of life. Yet, very little is known about how ethanol interacts with simultaneous associative learning acquired during postabsorptive periods. We have recently observed that preweanling rats avoid lemon odor previously paired with the intraoral infusion of a sapid sweet solution, a result likely to be caused by aversive consequences inherent to this procedure. Two experiments were conducted to analyze the effects of acute ethanol upon the acquisition of this avoidance response. Fourteen-day-old Wistar rats were intragastrically administered with ethanol (0.0, 0.25, 0.5, or 1.25 g/kg) and then exposed for 5 min to a lemon-scented chamber while being intraorally infused with sucrose (12% vol/vol). Four of such pairings were conducted immediately after ethanol administration. Control pups experienced these stimuli in an unrelated fashion. On postnatal day 15 animals were tested in a 5-min, two-way odor-preference test. Pups administered with vehicle during the acquisition phase exhibited a strong aversion to the lemon odor relative to control subjects. This avoidance response was reduced in pups that received 0.5 and 1.25 g/kg doses, whereas it completely vanished in those that received 0.25 g/kg dose. In a second experiment it was observed that, 10 min after the administration, blood ethanol concentrations attained with the 0.25, 0.5, and 1.25 g/kg doses were 11, 39, and 83 mg%, respectively. These data indicate that a very low dose of ethanol is able to counteract early aversive associative learning, a result likely to be mediated by anxiolytic properties of ethanol.

We have previously reported that withdrawal from acute ethanol (EtOH) exposure lowers mechanical thresholds in post-natal day 7 (P7) and post-natal day 21 (P21) rats. The present study tested the hypothesis that daily administration of 4 g/kg 15% EtOH for 5 days in rats during the human developmental equivalent of the third trimester, but not at a later time in development, would alter mechanical thresholds and formalin-induced pain behaviors. A transient decrease in mechanical thresholds (allodynia) was observed in P7 rats upon withdrawal from repeated EtOH between P3 and P7. When challenged with intraplantar formalin on P11, rats exposed to acute or chronic EtOH had enhanced phase II pain behaviors. In contrast to chronic EtOH administration to rats between P3 and P7, prolonged mechanical allodynia was observed in P21 rats upon withdrawal from chronic EtOH between P17 and P21. Formalin responses were unchanged in P25 rats exposed to acute or chronic EtOH. The affects of EtOH on somatosensory processing are dependent upon the age at which exposure occurs.

To characterize the effects of acute ethanol treatment on sexual motivation and performance, 30 male Long–Evans rats were assigned to one of three treatment conditions: saline ( n =9), 0.25 g/kg ethanol ( n =10), or 1.0 g/kg ethanol ( n =11). Males were injected intraperitoneally 30 min before behavioral testing. Male rats were placed in a multilevel testing chamber 5 min prior to the introduction of a receptive female rat and level changes were recorded as an index of sexual motivation. After the female rat was placed in the chamber, standard measures of sexual performance were recorded over three weekly tests. Results indicated that the highest dose of ethanol (1.0 g/kg) increased male rat level-changing behavior compared to the saline group. Although ethanol treatment failed to affect most measures of sexual performance, males administered 1.0 g/kg ethanol had fewer anogenital investigations and had longer postejaculatory intervals (PEIs) compared to control animals. The data from this experiment suggest that ethanol increases rodent sexual motivation but impairs specific parameters of sexual performance.

Effects of acute ethanol exposure during the prenatal phase of Bergmann glia cell (Bgc) generation were evaluated in three postnatal days. Ethanol exposed rats showed Bgc with reduced soma size, decreased number and width of their fibers, and increased fiber length, when compared with control animals. These differences, however, were significant at postnatal day 12. Our results demonstrate that acute, prenatal exposure to ethanol during critical stages of brain development disrupts Bgc early postnatal development.

The uptake of iron by the liver and cerebellum was measured in rats using [59Fe]transferrin. An acute ethanol load (50 mmol/kg body wt., i.p.) elicited a significant increase in the hepatic and cerebellar non-heme iron concentration. The uptake of 59Fe by the liver and the cerebellum was significantly greater in the ethanol-treated rats than in control animals. The administration of allopurinol prior to the ethanol load prevented the changes in liver and cerebellar non-heme iron content. Moreover pretreatment with allopurinol reduced the ethanol-induced enhancement of 59Fe uptake by the liver and completely prevented the changes in 59Fe uptake by the cerebellum. These effects of allopurinol lead us to suggest that oxygen-derived free radicals are involved in the ethanol-induced disturbances of iron uptake both at the hepatic and cerebellar level.

In rats, a complex longitudinal analysis of alcohol intake behaviour and electrophysiological sleep pattern was performed during different periods of stable voluntary alcohol consumption. By the sleep pattern, the existence of alcohol abuse and dependence development could be confifmed. Acute ethanol withdrawal was shown to be the obligatory and necessary element in alcohol abuse and dependence evaluation. The proposed behavioural and sleep pattern models might be used in the search for anti-alcoholic drugs in combination with the study of alcoholic aging processes.

Genetic differences in the hyperglycemic response to acute ethanol exposure and ethanol-induced conditioned taste aversion were examined using inbred mice. Adult male C57BL/6J and DBA/2J mice were injected with ethanol (0-6 g/kg, I.P.) and blood glucose levels determined over 4 h. C57 mice demonstrated greater dose-dependent elevations in blood glucose compared to DBA mice. In a conditioned taste aversion procedure, water deprived mice received ethanol injections (1-4 g/kg, I.P.) immediately after access to a NaCl flavored solution. DBA mice developed aversion to the ethanol-paired flavor at a lower dose (2 g/kg) than C57 mice. These results provide further support for a possible inverse genetic relationship between sensitivity to ethanol-induced hyperglycemia and sensitivity to conditioned taste aversion.

C57BL/6J mice were given five weeks of voluntary wheel running and then studied for behavioral impairment after an intoxicating dose of ethanol. Forty-four mice, 22 males and 22 females, were assigned to Wheel (free access to a running wheel in the home cage) or No Wheel conditions. At the end of the training period, animals were removed from the exercise cages and tested for noise avoidance after 2.4 g/kg ethanol (EtOH) or physiological saline (Sal). Mice could avoid 87.5-dB noise by entering and remaining in a randomly designated “safe corner.” In unexercised animals, EtOH caused a strong suppression on locomotor activity and avoidance behavior: No Wheel EtOH mice differed significantly from No Wheel Sal mice on both measures. In exercised animals, EtOH failed to cause significant suppression: Wheel EtOH animals did not differ significantly from Wheel Sal animals on either measure. The present results suggest that prior exercise training may be effective in offsetting the effects of acute ethanol intoxication.

Mice of different age groups (weanling, young adult and aged) were tested for changes in brain lipid- and protein-bound sialic acid (SA) 2 h after ethanol (2 g/kg, i.p.), either as a single dose or after binge dosing of five repeated doses of ethanol spaced 2 h apart. The results clarify our earlier demonstrations that acute ethanol can reduce whole brain SA. Ethanol generally decreased SA of both gangliosidic and glycoprotein origin, with the effect varying with number of doses and mouse age. Single-dose ethanol decreased both lipid-bound and protein-bound SA in young adults and decreased lipid-bound SA in aged mice. There was no effect on lipid-bound SA in weanlings, but weanlings did have a 72% decline in protein-bound SA. Repeated injections in young adults did not cause the SA decrease seen with acute injection. In both weanling and aged mice, however, repeated injections did cause large decreases in both lipid- and protein-bound SA. Small, but statistically significant, changes also occurred in free SA. Ethanol increased free SA in singly-dosed young adults and in multiply-dosed aged adults, while causing a distinct decrease in singly-dosed weanlings.

We read the findings of Krenz et al. [(1)][1]with great interest. Ischemic preconditioning remains one intriguing explanation for the association of moderate alcohol consumption with lower coronary mortality [(2)][2]and lower case-fatality rate of acute myocardial infarction (MI) [(3)][3]. Their

Myosin light chain kinase and pulmonary responses after acute ethanol exposure and burn injury Anita Zahs, Luis Ramirez, Melanie D. Bird, Jerrold R. Turner and Elizabeth J. Kovacs, Cellular and Molecular Biochemistry Program, Department of Surgery, Cellular and Molecular Biochemistry Program, Loyola University Medical Center, Maywood, IL USA, Department of Surgery, Loyola University Medical Center, Maywood, IL USA, Alcohol Research Program, Loyola University Medical Center, Maywood, IL USA, Department of Pathology, University of Chicago, Chicago, IL USA.

Antigen-specific CD8D T cell response are reduced by chronic ethanol and by TLR agonists: CD8D T cell alterations Prajwal Gurung, Jodi McGill, Betty M. Young, Ruth A. Coleman, Kevin L. Legge and Robert T. Cook, Department of Pathology, Carver College of Medicine, University of Iowa, Iowa City, IA USA, Interdisciplinary Graduate Program in Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA USA.