Biomedical subjects

N W Bond

Publications and source records attributed to N W Bond.

46 records · Page 3Linked to original sources

PubMed1973

Suppression of operant behavior and schedule-induced licking in rats.

The first experiment studied the effects of punishment on rats' lever pressing maintained by a fixed-interval schedule of food reinforcement and on the associated schedule-induced licking. When licking was followed by shock, licking was suppressed but lever pressing was largely unaffected. When lever pressing was followed by shock, lever pressing was suppressed but licking was unaffected. In both cases, the punished behavior recovered its previous unpunished level when the shocks were discontinued. In a second experiment, the rats' lever pressing was maintained by a variable-interval schedule of food reinforcement under which polydipsic licking also developed. Both lever pressing and licking were partially suppressed during a stimulus correlated with occasional unavoidable electric shocks. With a higher shock intensity, both behaviors were suppressed further. Both lever pressing and licking recovered their previous levels when shocks were discontinued. These results show that schedule-induced licking, which has been described as adjunctive behavior, can be suppressed by procedures that suppress reinforced lever pressing, an operant behavior.

Acoustic Stimulation↗

PubMedDate not supplied

The effects of chronic alcohol consumption or thiamin deficiency on radial-arm maze performance in the rat.

Experiment 1 tested the hypothesis that chronic consumption of ethanol, in the presence of good nutrition, is associated with impairments in memory. Rats were fed a vitamin-fortified ethanol-Sustagen diet with 35% ethanol-derived calories for 150 days. Two control groups were used. The first was pair fed a Sustagen mix in which sucrose had been substituted for ethanol. The second control group received ad lib access to standard laboratory chow and water. All animals were then placed on the chow and water diet for six weeks prior to testing in an eight-arm radial maze. There was a significant, but modest, difference between groups in the number of trials to reach a criterion level of seven correct from the first eight choices and all eight correct in ten choices. However, there were no differences between the groups when delays (0, 5, 20, 60, 120 and 240 minutes) were imposed between the 4th and 5th choices. In Experiment 2, a thiamin-deficient group was compared with pair-fed and ad lib control groups on the same task. The thiamin-deficient group took more trials to reach criterion but the groups did not differ in the delay testing phase. The results are discussed in the context of reference/working memory distinctions, and the literature on remediation of cognitive deficits associated with alcoholism.

Alcohol Amnestic Disorder↗

PubMedDate not supplied

Prenatal alcohol exposure and offspring hyperactivity: effects of physostigmine and neostigmine.

Rats were fed a liquid diet containing ethanol from days 6-19 of gestation. Controls were pair-fed the same diet with sucrose substituted for ethanol, or received ad lib chow and water. The activity of the offspring was observed at 10, 16, 22 or 28 days-of-age. Overall, offspring exposed to alcohol prenatally were hyperactive compared to controls at 16 and 22 days, but not at 10 or 28 days. Administration of physostigmine had no effect on the activity of any group at 10 days. At 16 days, physostigmine enhanced the activity of the alcohol group, had no effect on the sucrose group, but depressed the activity of the chow group. At 22 days it led to a dose-related decrease in activity in controls but had no effect on the activity of the alcohol treated pups. At 28 days, physostigmine decreased the activity of all three groups. Administration of the quaternary derivative, neostigmine, indicated that the effects of scopolamine at 22 days were probably central in origin. These data indicate that a putative cholinergic/inhibitory system becomes functional in control pups before 22 days, but in pups exposed to alcohol prenatally development is delayed by a number of days.

Age Factors↗

PubMedDate not supplied

Wernicke's encephalopathy and Korsakoff's psychosis: to fortify or not to fortify?

The conventional wisdom suggests that Korsakoff's psychosis, an amnesic disorder associated with prolonged alcohol consumption, is the chronic outcome of a thiamin deficiency first exhibited as Wernicke's encephalopathy. The present paper describes the debate in Australia over whether flour and alcoholic beverages should be fortified with thiamin, in an attempt to prevent Wernicke's encephalopathy and thus Korsakoff's psychosis. We conclude that the scientific evidence linking Wernicke's encephalopathy and Korsakoff's psychosis is tenuous. Certainly, it is not sufficient to support what would amount to mass medication.

Alcohol Amnestic Disorder↗

PubMedDate not supplied

Effects of dietary restriction on radial-arm maze performance and flavor memory in aged rats.

Two groups of aged rats, a dietary restricted group fed approximately 10 g per day from 6 weeks of age and a group fed ad lib throughout their life span, were compared with a young adult group on an 8-arm radial maze and a flavor memory task. The young adult displayed efficient performance on the radial-arm maze within the 15 day test period. In contrast, both aged groups exhibited significantly poorer performance in the maze in comparison with the young adult group neither aged group differed from chance at the end of the 15 days. The flavor memory task required the animals to consume a novel flavor. Their loss of neophobia, as indexed by their subsequent consumption, was then taken as an indication of the extent to which they remembered the novel flavor and its effects. The young adult group lost their neophobia more rapidly than either of the aged groups, which did not appear to differ from each other. Taken together, this pattern of results indicates that dietary restriction does not protect animals from the memory loss observed in aged animals.

Animals↗

PubMedDate not supplied

The effects of single and repeated episodes of thiamin deficiency on memory in alcohol-consuming rats.

The underlying pathogenesis of Korsakoff's syndrome, an amnesic disorder most commonly found in alcoholics, is not well understood. Chronic alcoholism is associated with thiamin deficiency and current thinking is that this may be the causal factor. In Experiment 1, rats were given a 20% (v/v) ethanol/water mix as their only source of fluid for 156 days. Three groups were made thiamin deficient through the combination of a thiamin-deficient diet and the centrally acting thiamin antagonist pyrithiamin hydrobromide, after 4, 15, and 26 weeks exposure to ethanol, respectively. The control group was given ad lib access to laboratory chow and water throughout this period. There were no differences between groups on either the working or reference versions of the Morris water tank paradigm. In Experiment 2, to test the hypothesis that a single bout of thiamin deficiency, with or without concurrent alcohol intake, is not sufficient to cause severe memory impairments, two groups of rats were subjected to three bouts of thiamin deficiency. One of these groups consumed an ethanol/water mix, the other tap water. A third group was made thiamin deficient on only one occasion. The control group was not made thiamin deficient and consumed lab chow and tap water throughout. Once again, there were no between-group differences in the data derived from testing in either the eight-arm radial maze or the Morris water tank task. These experiments indicate that the aetiology of Korsakoff's syndrome is more complex than previously thought.

Alcohol Drinking↗

PubMedDate not supplied

Prenatal alcohol exposure and offspring hyperactivity: effects of para-chlorophenylalanine and methysergide.

Pregnant Wistar rats were exposed to either a liquid diet containing ethanol, pair-fed an identical diet with sucrose substituted for ethanol, or received ad lib chow and water, during days 6-19 of gestation. Pups were injected with a dose of 100 mg/kg of para-chlorophenylalanine, 48 hr, 24 hr or immediately prior to activity testing at 16, 22 or 28 days of age. Further groups were injected with isotonic saline just prior to activity testing. Pups exposed to alcohol prenatally were more active than controls at 16 days of age. parachlorophenylalanine brought about significant increases in activity when injected 24 or 48 hr prior to testing in 16-day-old pups, and significant increases in activity when injected 24 hr prior to testing in 22- and 28-day-old pups. However, these effects of parachlorophenylalanine were similar regardless of prenatal treatment. In a second study, 16-day-old pups received saline, 0.5, 1.0 or 2.0 mg/kg of methysergide immediately prior to an activity test. Methysergide brought about a dose-related decrease in activity in all three groups of pups. Most importantly, the effects on activity of the methysergide were similar regardless of the treatment received during gestation. These data indicate that the hyperactivity associated with fetal alcohol exposure is unlikely to result from alterations in the ontogeny of a serotonergic system involved in response inhibition.

Age Factors↗

PubMedDate not supplied

Prenatal ethanol exposure and hyperactivity in rats: effects of d-amphetamine and alpha-methyl-p-tyrosine.

Pregnant Wistar rats were exposed to either a liquid diet containing ethanol, pair-fed an identical diet with sucrose substituted for ethanol, or received ad lib chow and water, during days 6-19 of gestation. The activity of their offspring was tested at 10, 16, 22 or 28 days of age. Pups exposed to alcohol prenatally were more active than controls at 16 and 22 days of age. Thirty min after being placed in the activity chamber, the pups were injected with either 0, 0.5, 1.0 or 4.0 mg/kg of d-amphetamine sulphate, and returned to the chamber for a further 120 min. Amphetamine brought about a dose-related increase in activity at 10, 22 and 28 days. At 16 days, peak activity was associated with the 0.5 mg/kg dose, activity declining at the higher doses. In a second study, pups received injections of 0, 25, 50 or 100 mg/kg of alpha-methyl-p-tyrosine (AMPT). Activity was unaffected by AMPT at 10, 22 or 28 days of age, but was increased at 16 days of age by the 25 and 50 mg/kg doses. Importantly, the time courses of the effects on activity of both d-amphetamine and AMPT were the same regardless of the treatment received during gestation. These data indicate that the hyperactivity associated with fetal alcohol exposure is not a result of alterations in the ontogeny of the catecholamine systems involved in arousal.

Animals↗

PubMedDate not supplied

Prenatal alcohol exposure and offspring hyperactivity: effects of scopolamine and methylscopolamine.

Rats were fed a liquid diet containing alcohol from days 6-19 of gestation. Controls were pair-fed the same diet with sucrose substituted for ethanol, or received ad lib chow and water. The activity of the offspring was observed at 10, 16, 22 or 28 days of age. Offspring exposed to alcohol prenatally were hyperactive compared to controls at 16 and 22 days, but not at 10 or 28 days. Administration of scopolamine had no effect on activity in any group at 10 days. At 16 days it reduced activity in the alcohol treated offspring but had no effect on the controls. At 22 days it led to a dose-related increase in activity in controls but had no effect on the already high levels of activity in the alcohol treated pups. At 28 days, scopolamine increased activity in all three groups. Administration of the quaternary derivative, methylscopolamine, indicated that the effects of scopolamine at 22 and 28 days were probably central in origin. These data indicate that a putative cholinergic/inhibitory system becomes functional in control pups before 22 days, but in pups exposed to alcohol prenatally development is delayed by a number of days.

Analysis of Variance↗

PubMedDate not supplied

Prenatal exposure to ethanol: association between increased gestational length and offspring mortality.

Pregnant Wistar rats were fed a nutritious liquid diet containing 35% ethanol-derived calories through days 6-19 of gestation. Control dams were pair-fed an identical liquid diet except for isocaloric substitution of sucrose for ethanol or ad lib laboratory chow and water. Ethanol exposure had no influence on the number of dams carrying their pregnancy to term but did lengthen the gestation period. The groups did not differ in litter size or weight at birth. However, there were significantly more still births in the litters of the ethanol-treated dams and more of their offspring died during the first 10 days of life. Within the group of dams fed ethanol there were significant associations between the length of gestation and the number of stillbirths and postnatal deaths.

Animals↗