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The effects of drinking ethanol throughout a lifetime on voluntary drinking behavior and ethanol-induced motor impairment were studied in alcohol-preferring AA (Alko, Alcohol) and alcohol-avoiding ANA (Alko, Non-Alcohol) rats of both sexes. At the age 3 months, the rats were tested for individual voluntary ethanol (10% vol./vol.) intake and ethanol-induced motor impairment (2 g/kg, i.p.). The rats were housed in group cages, half of them having 12% (vol./vol.) ethanol as the only source of fluid and the other half having free access to water. Food was always available for all animals. At the age of 23 months, their individual voluntary ethanol intake and ethanol-induced motor impairment were tested again. During forced drinking, the females of both strains consumed more ethanol than did the males. The ethanol consumption of the AA and ANA females and the ANA males increased significantly (P < .001) with age, but a slight decrease was seen in the ethanol consumption of the AA males. Time x strain interaction showed a significant (P < .05) difference in the ethanol consumption of male rats, with the AA males having a slight decrease in ethanol consumption with age, whereas the ANA males increased their ethanol consumption. After 19 months of forced ethanol exposure, AA males significantly decreased their individual voluntary ethanol consumption, and individual voluntary ethanol consumption by ethanol-exposed AA males was more pronounced (P < .001) than that of the AA rats that had free access to water (P < .05). For the female AA rats, those having free access to water significantly decreased their voluntary ethanol consumption (P < .05), but those having ethanol only did not. No significant changes in voluntary ethanol consumption with age or with different exposures were seen in the ANA rats. Body weights were higher in the groups having access to water than in the ethanol-only groups, but the differences were not significant within the AA and ANA strains. The ANA rats were significantly heavier in all groups. These results indicate that the voluntarily nondrinking ANA rats can drink almost as much ethanol as the voluntarily drinking AA rats when they are forced to drink ethanol and that lifelong forced ethanol drinking does not change their inherent drinking habits. When sensitivity to ethanol was measured with the tilting-plane test, the old AA female rats were more sensitive to ethanol than were the young ones. The young ANA females were more sensitive than the AA females when tested at 4 months. In males, aging did not produce any differences in ethanol sensitivity.

In a recent study, the mismatch negativity (MMN) component of auditory event-related potential, elicited by occasional frequency changes in a repetitive tone, was strongly attenuated by a low dosage of alcohol. We investigated the phenomenon in nine subjects with two different dosages of ethanol (0.35 and 0.55 g/kg), and with two magnitudes of frequency changes (5% and 10%), in a single-blind, placebo-controlled paradigm. Ethanol had no observable effect on the N1 and P2 deflections, nor on the reaction time to frequency changes measured in a separate session. However, the MMN was attenuated after administration of the larger dosage of alcohol, suggesting impaired preconscious processing of stimulus features outside the scope of attention. The results support the view according to which the automatic functions of human information processing are more sensitive than the controlled functions to the detrimental effects of alcohol. The fact that the MMN suppression was stronger when stimulus deviation was smaller indicates that at relatively low blood alcohol concentrations the detection of small deviations is especially hampered.

We have previously shown that an acute ethanol dose (1 g/kg), sufficient to impair the performance of a healthy rabbit, also reversibly depresses the activity of those limbic-cortex neurons that are specifically activated during recently learned behavioral acts. Our new morphological and neurophysiological data suggest a death of such neurons after 9-month chronic ethanol treatment. The effect of acute ethanol administration on neurons and performance speed in alcoholic rabbits was opposite to that found in healthy animals. Our results help to understand why neurocognition of alcoholics changes and why acute low-level alcohol ingestion influences them differently than healthy individuals.

Glutamate receptors are important target molecules of the acute effect of ethanol. We studied ethanol sensitivity of homomeric GluR-D receptors expressed in human embryonic kidney 293 cells and examined whether recently discovered transmembrane alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor regulatory proteins (TARPs) affect ethanol sensitivity. Coexpression of the TARPs, stargazin, and gamma4 increased the time constant (tau-value) of current decay in the presence of agonist, thus slowing the onset of desensitization and increasing the steady-state current. Ethanol produced less inhibition of the peak current than the steady-state current for all types of the GluR-D receptors. In addition, ethanol concentration-dependently accelerated the rate of desensitization, measured as the tau-value of fast decay of peak current. This effect was enhanced with coexpression of TARPs. The recovery from desensitization was slowed down by coexpression of gamma4 but ethanol did not affect this process in any GluR-D combination. The results support the idea that increased desensitization is an important mechanism in the ethanol inhibition of AMPA receptors and indicate that coexpression of TARPs can alter this effect of ethanol.

In this experiment we studied the effects of aging and lifelong ethanol consumption on rat peripheral sympathetic neurons. The aim was to find out the possible differences in the vulnerability to ethanol-induced neuronal degeneration between rats of both genders, or between the alcohol-avoiding (ANA) and the alcohol-preferring (AA) lines of rat. The superior cervical ganglia (SCG) of 40 male and 41 female AA and ANA rats were analyzed. The ethanol-exposed groups had 12% ethanol as the only available fluid from 3 to 24 months of age. The young (3 months) and old (24 months) control groups had water instead. SCG neuronal density, volume, and total neuron number were measured by unbiased morphometric methods. No gender difference was seen in either the volume of the SCG or in the SCG neuron number. The volume of the ganglion was significantly increased with age, but the total neuron number did not change. Neuronal density was significantly decreased with age, but lifelong ethanol consumption induced no further decrease. SCG neuron number in the ethanol-exposed groups did not differ from the age-matched or young control groups, but a significant negative correlation (r = -0.70, p<0.01) was seen between individual ethanol consumption and the number of SCG neurons in the female rats. The amount of lipopigment in the SCG was increased in the ethanol-exposed male rats. These results suggest that the peripheral sympathetic neurons are rather resistant to ethanol-induced degeneration, and that no major gender or line differences exist in this respect.

Rat pups were treated with monoamine uptake inhibiting antidepressant drugs, desipramine, imipramine or nomifensine (5 mg/kg) during the second and third postnatal weeks, and their later behavioral "despair," measured by Porsolt's swim test, was examined. At the age of two months, the desipramine-treated rats showed lengthened immobility in the swim test, and thus probably increased behavioral "despair." They also responded to 1 g/kg alcohol by shortening the immobility to the level of control rats. Neonatal treatment with either imipramine or nomifensine did not affect the swim test behavior. The results suggest that a low, stimulatory dose of alcohol was able to reverse the lengthened immobility in the swim test of rats treated with desipramine during the early postnatal period.

Directional asymmetry, the systematic differences between the left and right body sides, is widespread in human populations. Changes in directional asymmetry are associated with various disorders that affect craniofacial development. Because facial dysmorphology is a key criterion for diagnosing fetal alcohol syndrome (FAS), the question arises whether in utero alcohol exposure alters directional asymmetry in the face. Data on the relative position of 17 morphologic landmarks were obtained from facial scans of children who were classified as either FAS or control. Shape data obtained from the landmarks were analyzed with the methods of geometric morphometrics. Our analyses showed significant directional asymmetry of facial shape, consisting primarily of a shift of midline landmarks to the right and a displacement of the landmarks around the eyes to the left. The asymmetry of FAS and control groups differed significantly and average directional asymmetry was increased in those individuals exposed to alcohol in utero. These results suggest that the developmental consequences of fetal alcohol exposure affect a wide range of craniofacial features in addition to those generally recognized and used for diagnosis of FAS.

The effect of chronic ethanol intake and warm acclimation on the heat tolerance of rats under the influence of alcohol was studied. The animals were divided into two groups: Group 1 received water as their fluid intake and, group 2 received a 10% ethanol solution, and both groups were exposed to a temperature of 30 degrees C for 4 weeks. Excretion of urinary catecholamines was measured prior to warm exposure at 22 degrees C and once a week during warm exposure at 30 degrees C. After warm acclimation a dose of alcohol 2 g/kg was injected in the rats intraperitoneally (i.p.), and then they were exposed to a heat stress of 40 degrees C for 45 min. During warm acclimation, the controls consumed more fluid and they excreted more norepinephrine into the urine than the alcohol-fed animals during the first week. After the period of acclimation there were no significant differences in urinary excretion of catecholamines between the groups. Colonic temperature of the controls was 0.7 degrees C higher than in the alcohol-fed animals. Acute alcohol administration (2 g/kg) increased the colonic temperature of the alcohol-fed animals during a heat stress of 40 degrees C more than in the controls. After heat stress, the concentration of catecholamines in the blood was significantly higher in the controls. The results show that the hyperthermic effect of ethanol was more considerable in the rats whose drinking water during warm acclimation was an ethanol solution.