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Biomedical subjects

E P Riley

Publications and source records attributed to E P Riley.

At least 73 records · Page 4Linked to original sources

Social play in juvenile rats prenatally exposed to alcohol.

Offspring of rat dams that consumed isocaloric liquid diets containing either 35% or 0% ethanol-derived calories (EDC) from gestation days 6-20 were tested for play-fighting behavior as juveniles. Offspring from a group of dams maintained on standard lab chow and water throughout gestation were also included. Animals were tested in pairs, with offspring from each of the three prenatal treatment conditions (35% EDC, 0% EDC, and lab chow) being paired with another same-sex animal from one of these three prenatal treatment groups. Although play-fighting in juveniles is normally sexually dimorphic, this normal pattern was absent in juveniles prenatally exposed to alcohol. Male alcohol-exposed offspring displayed feminized behavior while female alcohol-exposed offspring showed masculinized behavior. This reversal of the normal sexually dimorphic aspects of play suggests that some of the behavioral disturbances associated with prenatal alcohol exposure may result, in part, from an alcohol-induced disruption of the hormonal environment in which the fetus develops.

Animals↗

Differential effects of prenatal exposure to alcohol on activity and circling behavior in rats.

The effects of prenatal exposure to alcohol on behavioral correlates of catecholaminergic function were examined in three experiments. In each experiment, subjects had one of 3 prenatal treatment histories: prenatal alcohol-exposed (35% ethanol-derived-calories, 35% EDC), nutritional control (0% ethanol-derived calories, 0% EDC) or standard control (lab chow, LC). In the first experiment, juvenile (33 to 59 days of age) female rats were tested for 16 hours overnight in standard rotometers. Subjects in the 35% EDC group were more active compared to both control groups, who did not differ from each other. However, the degree of circling (rotation) was not altered by prenatal exposure to alcohol. Since there was a positive correlation between age and rotation in the LC group, but not in the other 2 groups, adult female rats were similarly tested overnight in the rotometer. Again, circling behavior was not differentially affected by prenatal exposure to alcohol. Total overnight activity was no longer significantly greater in the adult 35% EDC group, although their initial activity was higher than that of the LC control group. In the third experiment, subjects from Experiment 2 were administered d-amphetamine (1.25 mg/kg) and tested in the rotometer for 1 hour. Both rotation and activity were increased by d-amphetamine, but there was not a significant interaction with prenatal alcohol exposure. Since rotation is a reflection of the intrinsic asymmetry of the nigrostriatal system, these results suggest that prenatal exposure to alcohol does not alter the development of this asymmetry.

Animals↗

Spontaneous fetal behavior after maternal exposure to ethanol.

Acute and chronic intubations of ethanol to pregnant rats produced changes in spontaneous fetal behavior four hours later. Fetuses from mothers in intermediate alcohol groups (4 and 6 g/kg) were substantially less active than controls (0 g/kg), but fetuses from low (2 g/kg) and high (8 g/kg) alcohol groups showed little indication of behavioral suppression. Circulating levels of alcohol in maternal blood, fetal homogenate and amniotic fluid at the time fetuses were observed confirmed that fetuses were exposed to alcohol in utero, but the measured concentrations of alcohol were not predictive of fetal activity. We suggest that some of the developmental consequences of Fetal Alcohol Syndrome may be the consequence of fetal inactivity induced by alcohol in utero.

Amniotic Fluid↗

The effect of prenatal alcohol exposure on umbilical cord length in fetal rats.

Umbilical cord length is reported to be a good indicator of fetal movement. This study was designed to examine the effects of chronic alcohol exposure on umbilical cord length in fetal rats. Exposure to alcohol during prenatal development was associated with shortened umbilical cord length, relative to controls. This finding was not a function of body weight differences alone and provides evidence that fetal movements may be decreased as a consequence of maternal alcohol consumption. The possible role of suppressed fetal movements in some of alcohol's teratogenic actions is also discussed.

Animals↗

Taste aversion learning in preweanling rats exposed to alcohol prenatally.

The effects of prenatal alcohol exposure on the development of a conditioned taste aversion were examined in preweanling rat pups. Mothers of these pups were fed isocaloric liquid diets containing either 35 or 0% ethanol-derived calories (EDC) from gestation days 6 through 20. A pair-feeding procedure was employed, and an ad lib lab chow control group was also included. At 5, 10, or 15 days of age, pups were infused with a saccharin solution through a cannula implanted in the oral cavity. Half of the pups in each group were then injected with lithium chloride (LiCl), which served as the poisoning agent, and the other half with sodium chloride (NaCl) as a control. Animals were subsequently tested for a conditioned aversion to the saccharin solution. At 15 days of age, all of the pups in the LiCl-poisoned group demonstrated a conditioned taste aversion to the saccharin solution, but the degree of this aversion was less in alcohol-exposed offspring. At 10 days of age, a taste aversion was learned, although it was not as strong as that shown by 15-day-old pups, and it appeared to be learned equally well by all of the prenatal treatment groups. At 5 days of age, there was marginal support for taste aversion learning. Again, it did not interact with prenatal treatment. The ontogenic differences in taste aversion learning exhibited by alcohol-exposed offspring relative to controls are discussed in terms of altered hippocampal development.

Animals↗

Ontogeny of suckling behavior in rats prenatally exposed to alcohol.

The effect of prenatal alcohol exposure on nipple attachment behavior was studied at a number of ages in rat pups whose mothers consumed liquid diets containing 35% or 0% ethanol-derived calories (EDC) or standard lab chow during pregnancy. In the first experiment, nondeprived pups were tested in groups of three (one from each of the prenatal treatment groups) for nipple attachment to an anesthetized lab chow dam. The second experiment examined the influence of the type of test dam (35% EDC, 0% EDC, or lab chow) on nipple attachment behavior. Finally, experiment three evaluated the possibility that the data from the preceeding experiments were the result of either testing the offspring in triads or alcohol-induced alterations in maternal behavior. Rat pups from all three groups reared by their biological mothers and a group of 35% EDC offspring fostered at birth to lab chow surrogate mothers were tested alone rather than in triads. The data from all three experiments clearly indicated an age-related pattern of nipple attachment behavior; the latency to attach was shortest in 6- to 12-day-old pups and increased rapidly from 13 to 21 days of age. Prenatal exposure to alcohol significantly increased the latency to attach to the nipple and the rank order of attachment at the younger ages (three to nine days of age) but not in the older animals. Also, the prenatal effect of alcohol was independent of the type of dam to which testing was conducted, the social interaction involved in testing triads, or fostering procedures. These results suggest that prenatal alcohol exposure can interfere with the development of normal suckling behavior, which might influence normal growth.

Age Factors↗

Evidence for a serotonergic mechanism of the learned helplessness phenomenon.

The present experiments examined the role of the serotonergic system in the learned helplessness phenomenon. In Experiment 1, a 200 mg/kg dose of 1-tryptophan injected 30 min prior to testing disrupted acquisition of Fixed Ratio 2 shuttle escape behavior. In Experiment 2, a 100 mg/kg dose of 5-HTP produced interference with the acquisition of the escape response. Furthermore, this interference was prevented by treatment with the serotonergic antagonist methysergide. In Experiment 3, animals were pretreated with a subeffective dose of 1-tryptophan in combination with subeffective exposure to inescapable shock. These animals showed a deficit in the acquisition of FR-2 shuttle escape. In Experiment 4, combined exposure to a subeffective dose of 5-HTP and inescapable shock (40 trials) resulted in an acquisition deficit. This deficit was reversed by methysergide. Experiment 5 showed that the detrimental effects of exposure to prolonged (80 trials) of inescapable shock can be prevented by treatment with methysergide. These studies implicate the serotonergic system as a possible mediator of the learned helplessness phenomenon.

Animals↗

Prenatal alcohol exposure: current issues and the status of animal research.

Animal studies of the tetratogenicity of alcohol have proliferated during the past few years. The purpose of this state-of-the-art is to overview some of the issues that the researchers have studied, to address methodological problems inherent in studies in this area, and to suggest directions for future research.

Abnormalities, Drug-Induced↗

Avoidance behavior in rats selectively bred for differential alcohol sensitivity.

"Most affected" (MA) and "least affected" (LA) rats, bred for extremes in motor impairment following an alcohol challenge, differed in their performance on two active avoidance tasks. In two-way shuttle avoidance, the MA line performed significantly better than the LA group, both in terms of response latencies and percent avoidances. The inferior performance of the LA line persisted across the 15 days of testing, and appeared to reflect an difference in asymptotic performance levels. In one-way avoidance, the MA line showed significantly better acquisition than the LA group; however, this difference dissipated across the 3 days of training. When tested following alcohol administration in either the one- or two-way avoidance paradigm, the MA rats showed a greater performance deficit than LA animals. These data were interpreted as indicating the generality of alcohol-related line differences to a situation motivated by aversive consequences. Moreover, the line difference in avoidance acquisition represents one of the few non-drug-related phenotypic differences that have been found in these lines. In previous generations, disparate base rates of wheel running have been reported, and the data presented here confirm and extend this finding.

Animals↗

Department of Psychology, State University of New York at Albany.

The effects of prenatal alcohol on learning and retention of passive avoidance and discriminated shock escape were examined in offspring of rats who consumed isocaloric liquid diets containing either 35, 17.5 or 0% ethanol derived calories (EDC) or lab chow during pregnancy. Alcohol exposed progeny required more trials to reach criterion during passive avoidance acquisition and had shorter second trail latencies into the shock compartment than did controls. Both these measures were found to be direct functions of prenatal alcohol exposure. No differences between groups were evident during retention testing (1, 3, or 7 days later). During the 25 trial acquisition phase of T-maze escape, alcohol exposed progeny made more errors despite equivalent group performance by the end of training. During retention testing 24 hours later, these offspring again evidenced more errors regardless of whether or not the original contingencies were reversed. Both learning and retention deficits in the T-maze were directly related to the percent EDC consumed by the mother during pregnancy.

Analysis of Variance↗

Lack of response inhibition in rats prenatally exposed to alcohol.

Offspring of mothers who consumed either 32, 19, 8, or 0% of their daily caloric intake in the form of ethanol during pregnancy were tested for passive avoidance. At 18 days of age, the number of trials to criterion and the within-group variability were direct functions of the amount of ethanol consumed by the mother during pregnancy. At 41--53 days of age, alcohol-treated pups still required more trials to criterion than controls and had faster speeds into the shock compartment on the first trial. When the progeny of mothers consuming either 35, 17, or 0% ethanol-derived calories during pregnancy were compared for conditioned taste aversion to a lithium chloride solution, a linear dose-response function was again evident. Animals in the alcohol-treated groups showed less suppression of drinking than controls. These investigations indicated that the effects of alcohol exposure in utero were manifested in behavioral outcomes involving response inhibition that were not correlated with the more familiar physical symptoms.

Animals↗

Hypnotic susceptibility to various depressants in rats selected for differential ethanol sensitivity.

MA rats, bred for greater motor impairment following subhypnotic doses of ethanol, were found to be more sensitive to the hypnotic effects of phenobarbital and chloral hydrate than were LA rats. In addition, the previously reported finding of a difference between the two lines of rats in duration of loss of righting reflex following a hypnotic dose of ethanol was replicated. The results are discussed in terms of a phenotypic difference in central nervous systems sensitivity to a range of sedative-hypnotics.

Animals↗

Nose-poking and head-dipping behaviors in rats prenatally exposed to alcohol.

In three experiments pregnant female rats consumed liquid diets containing various amounts of the total calories in the form of ethanol. In the first study, offspring of these females were tested in a nose-poking paradigm. The frequency of this response was found to be a direct function of the level of alcohol exposure in utero. In a second study when nose poking produced the onset of a dim light, animals prenatally exposed to alcohol were again found to poke more often, and this effect was not attenuated by preweanling handling. Finally, the generality of these findings became evident when head dipping rather than nose poking was examined; head-dip frequency was higher in alcohol-exposed offspring, and this effect was independent of stimulus complexity. Additionally, offspring body weights and survival rates following this prenatal alcohol exposure are presented.

Aging↗

Response perseveration in rats exposed to alcohol prenatally.

Pregnant female rats consumed liquid diets containing either 35, 17, or 0% of the total calories as ethanol. Offspring of these females were tested for spontaneous alternation at 21 days of age and for reversal learning in a T-maze shock-escape paradigm at 20--21 days of age. In the spontaneous alternation test, rats exposed to alcohol prenatally took more trials than controls to enter the goal compartment opposite to that initially entered. In the T-maze escape study, alcohol-exposed offspring made more mistakes prior to criteron and more mistakes per trial than controls when the previously incorrect goal was made safe during reversal learning. In both studies linear dose-response functions were found. Furthermore, there was a significant tendency for the within-group variabitliy to increase as the level of prenatal exposure increased, perhaps indicating that the incidence as well as the severity of behavioral dysfunction was dose dependent. The results are interpreted in terms of a delay in the development of a central inhibitory system.

Animals↗

Differential tolerance to pentobarbital in rats bred for differences in alcohol sensitivity.

Two lines of rats bred for differences in motor impairment following alcohol treatment were also found to be differentially affected by sodium pentobarbital in three experiments. The most affected (MA) animals, bred for sensitivity to alcohol, showed a decrement in stabilimeter activity at doses of 8 mg and 16 mg pentobarbital per kg body weight. The least affected (LA) animals, bred for insensivity to alcohol, were affected only by the higher dose, at which the resulting impairment was still less than that of the MA group. This finding was partially replicated in a second study designed to test the possibility of an activating effect of pentobarbital on LA animals at 8 mg/kg. In a final study, MA animals were more likely to lose their righting reflex than LA animals at a dose of 18 mg/kg, and 'slept' longer following this dose. These results indicate that the differential sensitivity shown by these animals is not specific to alcohol, but can be generalized to another depressant.

Animals↗

Selective breeding of rats for differences in reactivity to alcohol: an approach to an animal model of alcoholism. III. Some physical and behavioral measures.

The results of selective breeding for differential impairment of motor activity after alcohol injection is shown for the first 13 generations of the LA and MA rat strains. In F13 rats, the mean decrement of activity after 1.5 g ethanol per kg i/p. is 90% for MA rats and 42% for LA rats, the strain difference significant at a "p" of 1.8 x 10(-11). Blood alcohol levels, body weight, litter size, organ weights and induction of taste aversion to alcohol and lithium chloride are described for these strains in various of the generations. Although strain differences are apparent on some of these measures, none are of a degree or kind which offers more than a speculative explanation of the large difference between the strains in their central nervous system sensitivity to alcohol.

Alcoholism↗