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Long-Evans and Sprague-Dawley rats show differential behavioral responses to cocaethylene, a metabolite derived from the simultaneous ingestion of ethanol and cocaine. Such differences may also be manifested when these outbred strains are exposed to ethanol and cocaine. To test this hypothesis, both strains were fed an ethanol-diet (8.7% v/v) in conjunction with cocaine (15 mg/kg) injections for 15 days. The following parameters were evaluated: (a) ethanol consumption, (b) cocaine-induced behavioral activity, (c) blood ethanol levels, (d) blood, liver, or brain cocaine and cocaethylene levels, and (e) liver catalase and esterase activity. We found that Long-Evans rats drank significantly more of the ethanol diet relative to the Sprague-Dawley line during the first few days of the test session. This rat phenotype also differed significantly from the Sprague-Dawley line in terms of behavioral activity after cocaine administration. Blood ethanol levels did not differ between strains. Similarly, we failed to detect strain-dependent differences in blood, liver, or brain cocaine levels as measured by gas chromatography/mass spectrometry. Cocaethylene levels, however, were higher in blood and brain of Long-Evans relative to Sprague-Dawley cohorts. Although the ethanol-cocaine regimen produced a marked suppression of catalase and esterase activity compared with control-fed rats, this suppression was roughly equivalent in both rat phenotypes. These data are discussed in the context of genotypic background and vulnerability to polysubstance abuse.

Ethanol exposure during fetal development can result in behavioral and neurological deficits, including reduced cognitive functions, retarded growth, and craniofacial abnormalities. Adenosine is an endogenous neuromodulator that fine-tunes the release and/or synaptic activities of several neurotransmitters, including glutamate, dopamine, and serotonin. Our aim was to determine whether ethanol exposure during early development affects adenosine receptors, particularly the A1 receptor subtype, in adult rats. Female rats were given water or 15% (vol/vol) ethanol in water prior to mating and throughout gestation and lactation. Sixty-day-old male rat offspring from these dams were randomly selected and assayed for adenosine A1 receptor expression in four brain areas: cortex, cerebellum, hippocampus, and striatum. Our results indicate that ethanol intake by dams decreased body and brain weights of offspring and reduced both A1 receptor mRNA and protein density in cortex and cerebellum. These preliminary findings indicate that ethanol intake by dams during pregnancy and lactation can affect adenosine A1 receptor signalling in the offspring. A pair-fed controlled study is warranted to explore these findings further.

AbstractThe present study was undertaken to assess the influences of chronic maternal ethanol consumption, prior to and during gestation, on the development of synaptic plasma membranes (SPMs) and on the synthesis of SPM glycoproteins in offspring. Comparisons were made between animals whose mothers were pair‐fed a control or 6.6% (v/v) ethanol liquid diet in which protein accounted for either 18% (original) (C & E) or 21% (revised) (*C & *E) of the calories. In addition, groups of pups that were either cross‐fostered (*C & *E) with chow‐fed surrogate mothers or reverse cross‐fostered (offspring of chow‐fed mothers with *C & *E mothers) were examined. Ethanol and matched (same dietary group) control pups had comparable brain and body weights, brain protein content, and yield of SPM proteins during the 10–24 day age period examined. However, the yield of SPM proteins from ethanol and control offspring of and/or reared by the three groups of rat mothers that received the *E and *C liquid diets was greater than that of the offspring of rats that were fed the original diets. This suggests that the original diets were not nutritionally adequate for pregnant rats. Despite the fact that the content of SPM proteins was comparable in ethanol and matched control pups, the offspring of ethanol‐treated rats had an abnormal distribution of [3H]‐or [14C]‐fucose‐derived radioactivity among SPM glycoproteins. The SPM abnormalities were most severe in the non‐cross‐fostered offspring of E rats. No SPM glycoprotein abnormalities were found in the reverse cross‐fostered group. The results of the present study demonstrate that chronic maternal ethanol consumption prior to parturition has a severe effect on the synthesis of SPM glycoproteins in developing offspring without affecting the content of SPMs per se. It also demonstrates the importance of optimizing the composition of liquid diets used to feed pregnant rats.

The type of alcoholic beverage consumed by pregnant drinkers appears to influence fetal outcome. Beer drinkers are at greater risk than consumers of other alcoholic beverages for having children with fetal alcohol effects (Sixth Special Report to the U.S. Congress on Alcohol and Health, 1987). The magnitude of the risk is increased, because beer is a very popular beverage in our society. Although animal models have been developed to mimic fetal alcohol effect in humans, it is possible that stressful procedures such as intubation, and the hunger of pair-fed animals matched to animals drinking ethanol in liquid diet have interfered with obtaining a pattern of alcohol intake which closely matches that of humans. A majority of the animal models used for alcohol studies have provided ethanol for intake, rather than alcoholic beverages such as beer, which is favored by humans. Thus, a new model for voluntary beer drinking by rats is presented here for use in the study of maternal beer drinking during gestation, and the subsequent developmental consequences in the offspring. Female Long Evans rats (N = 45) were tested by beer preference and assigned to beer drinking (BR) or control groups. All animals were given standard laboratory diet and water ad libitum. BR dams were provided ad libitum access to beer. A pair-fed group (PF) was given non-alcoholic beer with dextrin added to match the caloric intake of the BR animals. Control animals (CT) were given free access to food and water. Control groups included beer preferring animals as well as non-preferring animals.(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND Central pontine myelinolysis (CPM) includes symmetric demyelination of the central pons. CPM is a rare neurological disorder that generally develops after rapid correction of hyponatremia in individuals having underlying conditions, such as malnutrition, alcoholism, and severe burns. It can cause severe long-term disabilities. However, there is currently no pharmacotherapy capable of promoting remyelination, a process crucial for recovery from CPM. We present the case of a patient with alcoholism and malnutrition-related CPM, which developed following rapid correction of hyponatremia but then improved remarkably with supportive physical therapy. CASE REPORT A 44-year-old alcoholic and malnourished man was admitted to an emergency hospital for disorientation due to overdrinking, but later developed bulbar palsy after hyponatremia was unexpectedly, but rapidly, corrected. Axial scans of the diffusion-weighted brain MRI revealed a characteristic lesion known as a piglet sign in the central pons. Based on his underlying conditions, present episode of sodium correction, and MRI finding, the patient was diagnosed as having CPM, which progressively worsened, resulting in locked-in syndrome after 12 days. The patient was then transferred to a long-term care unit and received simple motion exercise daily, but no specific medication. His symptoms gradually improved, achieving discontinuation of tube feeding on day 21, independent walking on day 110, and discharge after 6 months. CONCLUSIONS This report highlights the importance of physical therapy, the potential of which is often underestimated despite its broad benefits for human health, as a readily applicable intervention for patients with CPM. Further understanding of mechanisms underlying exercise-induced myelination should contribute to establishing novel therapies for a wide spectrum of brain disorders.

BackgroundAdolescent alcohol abuse remains a serious public health concern, with nearly a third of high school seniors reporting heavy drinking in the previous month.MethodsUsing the high ethanol‐consuming C57BL/6J mouse strain, we examined the effects of ethanol (3.75 g/kg, IP, daily for 45 days) on body weight and brain region mass (cerebral cortex, cerebellum, corpus callosum) during peri‐adolescence (postnatal day [P]25 to 70) or adulthood (P180 to 225) of both males and females.ResultsIn control peri‐adolescent animals, body weight gain was greater in males compared with females. In the peri‐adolescent exposure group, ethanol significantly reduced body weight gain to a similar extent in both male and female mice (82 and 84% of controls, respectively). In adult animals, body weight gain was much less than that of the peri‐adolescent mice, with ethanol having a small but significant effect in males but not females. Between the control peri‐adolescent and adult cohorts (measurements taken at P70 and 225, respectively), there were no significant differences in the mass of the cerebral cortex or the cerebellum from either male or female mice, although the rostro‐caudal length of the corpus callosum increased slightly but significantly (6.1%) between these time points.ConclusionsEthanol treatment significantly reduced the mass of the cerebral cortex in peri‐adolescent (−3.1%), but not adult, treated mice. By contrast, ethanol significantly reduced the length of the corpus callosum in adult (−5.4%), but not peri‐adolescent, treated mice. Future studies at the histological level may yield additional details concerning ethanol and the peri‐adolescent brain.

This study was conducted to determine the temporal and regional vulnerability of the brain as a function of exposure to alcohol during brain development. Our goal was to manipulate the timing of alcohol exposure and assess the relative risk of cell loss in two different brain regions. Groups of timed pregnant Sprague‐Dawley rats received binge‐like alcohol exposure during either the first 10 days (first‐trimester equivalent) or second 10 days of gestation (second‐trimester equivalent), or the combination of first‐ and second‐trimester equivalents for prenatal treatments. Offspring from some of the animals exposed to alcohol during the combined first‐ and second‐trimester equivalent were reared artificially from postnatal days (P) 4 through 9 (part of the third‐trimester equivalent) and also received binge‐like alcohol during this period, producing animals that were exposed to alcohol during all three trimesters equivalent. Offspring from untreated dams were also reared artificially and received alcohol from only P4‐9, thus creating animals that were exposed to alcohol only during part of the third‐trimester equivalent. All pups were perfused on P10. Appropriate controls (nutritional and normally reared) were matched to every alcohol treatment combination. Peak blood alcohol concentrations were not different among the treatment groups for a given sampling time. Total cell numbers in the cerebellum (Purkinje and granule cells) and the olfactory bulb (mitral and granule cells) were estimated by the unbiased stereological technique, the optical disector. In terms of temporal vulnerability, alcohol exposure during the equivalent of all three trimesters resulted in a greater reduction in cerebellar Purkinje cell numbers compared with exposure to alcohol during the third‐trimester equivalent, whereas both groups had a significant reduction in cell number compared with all other timing groups. Cerebellar granule cell number was reduced after alcohol exposure during all three trimesters equivalent, compared with all other timing groups. Alcohol exposure during the third‐trimester equivalent resulted in a decrement in the number of olfactory bulb mitral cell numbers compared with all other groups, but there were no differences among the timing groups in numbers of olfactory bulb granule cells. When the cell loss in the two regions was compared within each alcohol treatment group to determine the relative regional vulnerability, the primary salient finding was that cerebellar Purkinje cells were more vulnerable to alcohol‐induced loss subsequent to exposure during all three trimesters equivalent. No other regional differences were detected. These results extend earlier findings by showing that alcohol exposure during different periods of brain development results in regional differences in cell loss as a function of the timing of alcohol exposure during brain development and illustrate the variability of alcohol‐induced neuronal loss.

A large evidence-based review on the effects of a moderate consumption of beer on human health has been conducted by an international panel of experts who reached a full consensus on the present document. Low-moderate (up to 1 drink per day in women, up to 2 in men), non-bingeing beer consumption, reduces the risk of cardiovascular disease. This effect is similar to that of wine, at comparable alcohol amounts. Epidemiological studies suggest that moderate consumption of either beer or wine may confer greater cardiovascular protection than spirits. Although specific data on beer are not conclusive, observational studies seem to indicate that low-moderate alcohol consumption is associated with a reduced risk of developing neurodegenerative disease. There is no evidence that beer drinking is different from other types of alcoholic beverages in respect to risk for some cancers. Evidence consistently suggests a J-shaped relationship between alcohol consumption (including beer) and all-cause mortality, with lower risk for moderate alcohol consumers than for abstainers or heavy drinkers. Unless they are at high risk for alcohol-related cancers or alcohol dependency, there is no reason to discourage healthy adults who are already regular light-moderate beer consumers from continuing. Consumption of beer, at any dosage, is not recommended for children, adolescents, pregnant women, individuals at risk to develop alcoholism, those with cardiomyopathy, cardiac arrhythmias, depression, liver and pancreatic diseases, or anyone engaged in actions that require concentration, skill or coordination. In conclusion, although heavy and excessive beer consumption exerts deleterious effects on the human body, with increased disease risks on many organs and is associated to significant social problems such as addiction, accidents, violence and crime, data reported in this document show evidence for no harm of moderate beer consumption for major chronic conditions and some benefit against cardiovascular disease.