Self-reported mood and drinking patterns following hospital treatment for alcoholism.
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Alcohol Drinking↗
Biomedical subjects
E P Riley
Publications and source records attributed to E P Riley.
Selective breeding of rats for differences in reactivity to alcohol. An approach to an animal model of alcoholism. II. Behavioral measures.
Two lines of rats have been bred which differ in sensitivity to alcohol over a range of doses, but the difference is not reflected in blood alcohol concentration, alcohol intake or selection. The two lines respond similarly on tests of emotionality; however, differences in running-wheel activity suggest differences in neural apparatus.
Alcohol Drinking↗
Polydipsic and home-cage fluid choices: the effects of sweetening.
When rats were offered a choice of alcohol, butanediol and noncaloric saccharin solutions in a home-cage situation, consumption of saccharin dominated fluid choice, whether or not the animals were deprived of food.
Alcohol Drinking↗
Assessment of alcoholics' moods at the beginning and end of a hospital treatment program.
The Profile of Mood States was administered weekly to 122 completers and 91 noncompleters of a hospital alcohol rehabilitation program. Ss' initial mood scores were not significant predictors of whether they would complete the program or of whether they would attain abstinence or show improvement in drinking practices at 3-month follow-up. When Ss left the program their final mood scores indicated significant improvement in mood states compared to their initial scores. Completers who later were found to be abstinent showed a trend toward affective improvement on all 6 Profile scales. It is suggested that assessment of an alcoholic's mood can contribute to formulation of treatment plans.
Alcohol Drinking↗
Selective breeding of rats for differences in reactivity to alcohol. An approach to an animal model of alcoholism. I. General procedures.
Strains of rats are being developed which have distinct responses in spontaneous locomotor activity to a subhypnotic dose of alcohol. The purpose is to produce one strain in which the injection of a standard dose of alcohol will result in objectively measurable intoxication and a second in which an identical dose will result in virtually no effect.
Alcoholic Intoxication↗
Effects of artificial rearing on electrophysiology and behavior in adult rats.
Maternal separation during crucial periods of development can lead to both physiological and behavioral sequelae. However, the exact consequences of maternal separation are paradigm dependent. The present study utilized complete artificial rearing (AR) to evaluate the effects of maternal separation on behavioral and electrophysiological functioning. In this procedure thermoregulation and weight gain progress are normal, but pups are deprived of any maternal influence from postnatal day 4 to 12. Artificial rearing was found to have no effect on EEG as assessed using spectral analyses. However, the N1 component of the auditory event-related potential (ERP) in artificially reared rats was significantly delayed. Artificial rearing had no effect on overall locomotor activity, but artificially reared rats were more behaviorally inhibited than suckled controls in the open field. This study suggests that artificial rearing or chronic maternal separation (24 h/day from PN4 to PN12), while not producing gross behavioral effects, can produce selective enduring alterations in neurosensory responses.
Animals↗
Effects of initial tolerance on acquired tolerance to alcohol in two selectively bred rat strains.
The extent to which initial sensitivity to alcohol influences acquired tolerance was investigated in two selectively bred rat lines. These two lines have been selectively bred for differences in initial sensitivity to alcohol. The most affected (MA) line shows about a 90% reduction in motor activity following a 1.5 g/kg dose of alcohol compared with only a 40% reduction in least affected (LA) animals. In an initial investigation using stabilimeter activity, MA animals demonstrated increased tolerance following regular alcohol exposure, while LA animals showed little change from their initial levels of tolerance. In a second study following a similar intubation procedure, tolerance was assessed by sleeping time. Both MA and LA rats evidenced increased tolerance to alcohol, although MA animals did not approach the levels of tolerance shown by LA animals. In both studies the amount of initial tolerance was correlated with the degree of acquired tolerance. The potential for using these animals in the study of the underlying mechanisms of tolerance is discussed.
Animals↗
Delayed taste aversion learning in preweanling rats exposed to alcohol prenatally.
Parallels between the behavioral profiles of rats exposed to alcohol prenatally and those with hippocampal damage suggest that hippocampal dysfunction may underlie some of the behavioral abnormalities resulting from prenatal alcohol exposure. Because of possible hippocampal involvement in the acquisition of a delayed conditioned taste aversion, this task was assessed in rat pups exposed to alcohol prenatally. Long-Evans rats were maintained on liquid diets containing either 35% or 0% ethanol derived calories from Days 6-20 of gestation. Pair-feeding procedures and an ad lib Lab Chow (LC) group were included. Fifteen-day-old offspring from these three groups were given access to saccharin and then injected immediately (0 hr) or 2 hr later with either lithium chloride (LiCl) or sodium chloride (NaCl). Immediate pairing of saccharin with LiCl produced a marked taste aversion, although this effect was less pronounced in 35% EDC pups. In the 2 hr condition, weaker aversions were exhibited and again the 35% EDC group showed the least aversion. However, prenatal treatment did not interact with the injection interval.
Animals↗
Effects of scopolamine on spontaneous alternation and shuttle avoidance in rats exposed to alcohol in utero.
The behavioral effects of the anticholinergic scopolamine were examined in rats exposed to alcohol prenatally. Pregnant Long-Evans rats received isocaloric liquid diets containing either 35% or 0% ethanol-derived calories on Days 6-20 of gestation. A pair-feeding procedure was used, and a lab chow control group was also included. In Experiment 1, adult offspring were tested on a spontaneous alternation task following 1 mg/kg scopolamine or saline. Independent of prenatal treatment, scopolamine caused an increase in the number of trials to alternate. In Experiment 2, offspring were tested on a two-way shuttle avoidance learning task following a 1 mg/kg injection of scopolamine or methylscopolamine. Alcohol-exposed animals injected with methylscopolamine made fewer avoidances than controls on the second day of testing while treatment with scopolamine enhanced avoidance performance to control levels. These data suggest that prenatal exposure to alcohol does not interfere with scopolamine-induced changes in the behavior of adult rats.
Animals↗
Effects of physostigmine on shuttle avoidance in rats exposed prenatally to ethanol.
Shuttle avoidance performance following pretreatment with physostigmine was assessed in 85- to 100-day-old rats whose mothers consumed a liquid diet consisting of 35% ethanol-derived calories (EDC) during pregnancy. Offspring of pair-fed (0% EDC) and ad lib lab chow (LC) dams served as controls. Animals received either 0, 0.1 or 0.2 mg/kg physostigmine sulfate prior to acquisition training in a shuttle avoidance apparatus. Training consisted of 50 trials/day for 4 days. Thirty-five percent EDC rats made fewer avoidances than controls during acquisition training. Treatment with physostigmine reduced the number of avoidances made, and did so similarly for all prenatal treatment groups. Escape latencies were not affected by prenatal treatment, although they were increased by physostigmine administration prior to training. Neither prenatal treatment nor physostigmine treatment affected activity as measured by the number of intertrial crossings while in the apparatus. These data indicate that alcohol-exposed animals did not respond differentially to physostigmine relative to controls, suggesting that cholinergic dysfunction may not underlie the prenatal alcohol-induced deficit in active avoidance.
Animals↗
Absence of differential motoric and thermic responses to clonidine in young rats exposed prenatally to alcohol.
We studied the involvement of altered noradrenergic function in the behavioral consequences of fetal ethanol exposure. Pregnant rats were fed a liquid diet containing 35% Ethanol-Derived Calories (EDC), pair-fed a 0% EDC diet with sucrose substituted isocalorically for ethanol, or fed ad lib lab chow. In Experiment 1, offspring from these prenatal treatment groups were injected with the alpha-adrenergic agonist clonidine (0.5 or 2.0 mg/kg) at 10 or 42 days of age and showed age-characteristic, dose-dependent increases in locomotor activity, exploration, forelimb treading, and catalepsy. In Experiment 2, offspring were injected with clonidine (0.25 or 1.0 mg/kg) at 10, 14, or 18 days of age, and locomotor activity and wall-climbing were observed in a warm chamber (33 degrees C). Catalepsy and rectal temperature were also scored. There were no significant differential effects of clonidine on any prenatal treatment group at any age for any measure of activity or rectal temperature. The results do not support the hypothesis that fetal ethanol exposure alters noradrenergic systems in behaviorally significant ways.
Aging↗
Prenatal ethanol alters gait in rats.
Rats exposed to ethanol in utero were assessed for changes in gait at 55 days of age. Ethanol-exposed animals had significantly shorter stride lengths, more open step angles, and less gait symmetry than control rats. There were no differences in stance width or apparent speed. This pattern of changes in motor function indicates that prenatal exposure to ethanol produces long-lasting "ataxia" in rats. These results closely resemble previous findings of altered gait following neonatal ethanol exposure in rats, as well as clinical findings in some FAS children. The results are consistent with an hypothesis of prenatal ethanol-induced disruption of functional hippocampal and/or cerebellar development. Ataxia and gait dysfunction may be sensitive indicators of ethanol teratogenesis.
Animals↗
Ethanol teratogenesis in mice selected for differences in alcohol sensitivity.
Long-Sleep (LS) and Short-Sleep (SS) mice, selectively bred for differences in ethanol-induced narcosis, were administered ethanol (2.9, 4.0, 4.5, or 5.0 g/kg) twice per day during the period of organogenesis. On gestation day 18, the dams were sacrificed and the uterine horns were examined for live, dead, and resorbed fetuses. Live fetuses were weighed and assessed for either skeletal or soft tissue anomalies. The 5.8 g/kg/day dose had no effect on prenatal mortality, litter size, body weight, or number of physical anomalies in either line. However, the alcohol-sensitive LS mice exposed to ethanol doses of 8.0 g/kg/day or more evidenced decreased body weights while weights for the alcohol-insensitive SS mice differed from controls at only the highest dose tested. The incidence of skeletal variants was increased in the LS mice exposed to the 10 g/kg/day ethanol dose. These results indicate genetically-mediated alcohol sensitivity increases susceptibility to some of the fetotoxic effects of in utero alcohol exposure.
Animals↗
Arginine vasopressin and body fluid homeostasis in the fetal alcohol exposed rat.
Studies involving fluid homeostasis were carried out in adult Long-Evans rats born to mothers given liquid diets containing 35% of the calories derived from ethanol and compared to offspring of dams given isocaloric liquid diets containing no ethanol. Plasma levels of arginine vasopressin (AVP), plasma and urine osmolality, and urine production were determined in water-sated and water-deprived offspring. In the water-sated condition, the group exposed to alcohol prenatally had plasma levels of AVP seven-fold above control levels. This increase was associated with a large increase in within-group variability. Water consumption was also significantly elevated in the group of fetal alcohol exposed (FAE) rats. Plasma and urine osmolality and urine production were similar to control levels. In the control animals, 24-hr of water deprivation produced the expected increase in AVP, in plasma and urine osmolality, and decrease in urine production. The FAE animals, however, showed parallel changes in plasma and urine osmolality and urine production with no significant change in AVP. Examination of basal glucose metabolic rates in the cerebral structures involved in fluid homeostasis revealed that despite the large increase in AVP levels in the FAE rats, only the neurohypophysis and supraoptic nuclei showed significant increases in activity. These data suggest that fetal alcohol exposure causes a long-term disruption in the central mechanisms regulating vasopressin release and fluid homeostatic responses.
Animals↗
Responses to ethanol challenge in long- and short-sleep mice prenatally exposed to alcohol.
Individual sensitivity to alcohol may influence the severity of functional deficits due to prenatal alcohol exposure. To examine this hypothesis, Long-Sleep (LS) and Short-Sleep (SS) mice, selectively bred for differences in ethanol-induced narcosis, were intubated with either 2.9 g/kg ethanol (E) or an isocaloric amount of sucrose (S) twice per day on days 7 through 15 of pregnancy. An untreated control group (C) was maintained for each line. Offspring were fostered to lactating Rockland-Swiss mice at birth. Males and females from each litter were challenged with an acute dose of ethanol (3.8 g/kg) at 30 days of age. Measures of sleep time duration, waking blood ethanol concentrations (BEC), rectal temperatures, heart rate, and ethanol clearance were obtained to examine whether the acute effects of ethanol are altered by prenatal alcohol exposure. Prenatal alcohol exposure did not differentially affect responses to ethanol challenge within either genotype. Ethanol-induced hypothermia, heart-rate depression, and sleep time did differ between genotypes, with LS more affected than SS mice. Ethanol clearance rates were faster for SS than LS mice. These results suggest postnatal pharmacological responses to acute ethanol challenge are not altered by prenatal alcohol exposure in LS and SS mice. Prenatal alcohol-exposed offspring of both mouse genotypes showed lower average heart rate responses than controls, suggesting this measure may be a sensitive indicator of prenatal alcohol effects in mice.
Animals↗
Recognition of food in weanling rats exposed to alcohol prenatally.
Offspring of rats fed a liquid diet containing ethanol during their pregnancies were compared to controls on a caloric discrimination test beginning at 22 days of age. All pups received simultaneous choice between a palatable, noncaloric diet and a similar diet containing starch. Each diet contained a distinctive flavor. To test for flavor preference learning, pups then received an extinction test: a simultaneous choice between two noncaloric diets, identical except for flavor. Prenatal alcohol exposure had no substantial effect on the caloric discrimination, and all groups preferentially ingested the starch diet on all test days. However, during the extinction test, alcohol-exposed pups showed a significantly weaker flavor preference than control pups. These data extend the effects of prenatal alcohol exposure on learning and ingestive behavior to include solid food discriminations at the time of weaning.
Analysis of Variance↗
The behavioral teratogenicity of alcohol is not affected by pretreatment with aspirin.
Prenatal alcohol exposure is associated with a variety of developmental abnormalities, including neuroanatomical, physical, and behavioral features. Several mechanisms for alcohol's teratogenic effects have been proposed. This study addresses the role of prostaglandins in the abnormal development that often occurs after maternal alcohol consumption. On gestation days 8 to 18, pregnant Sprague-Dawley rats were prenatally treated with 6 g/kg alcohol following pretreatment with 150 mg/kg aspirin. Behavioral testing of offspring included measures of open-field activity, exploratory behavior, passive avoidance, active avoidance, and acoustic startle response. In most cases, pretreatment with aspirin did not affect performance in alcohol-exposed or control rats.
Animals↗
Electrophysiological and behavioral findings in rats prenatally exposed to alcohol.
Clinical studies have shown that behavioral and electrophysiological abnormalities occur in some human infants born to alcoholic mothers. The present study used rats to evaluate the effects of prenatal ethanol exposure on locomotor behavior and two paradigms for the generation of auditory event-related potentials (ERPs). Pregnant rats were fed liquid diets, one group received alcohol and the other was a nutritional control. The offspring were allowed to mature prior to the electrophysiological and behavioral testing. Prenatal alcohol exposed rats showed significantly more locomotor behavior in the first 4 hours of their activity cycle than nonethanol exposed rats, although not over a subsequent 8-hour period. Evaluation of the electrophysiological data revealed that the prenatal alcohol exposed group had significantly longer latencies of their P1 and N1 ERP components, in the hippocampus, than the control group. These results support anatomical data suggesting that the hippocampus may be an important area in which to direct further study of what brain mechanisms may be altered by prenatal ethanol exposure in the rat.
Acoustic Stimulation↗