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Biomedical subjects

S J Cooper

Publications and source records attributed to S J Cooper.

At least 217 records · Page 12Linked to original sources
PubMed1982

Suppression of drinking and induction of sedation by a dopamine agonist is blocked by small doses of spiperone.

ET 495 (piribedil) produced significant hypodipsia in thirsty rats at 5 and 20 mg . kg-1, the effect being greater at the lower dose. At 5 mg . kg-1 ET 495 also induced a significant sedating effect, a characteristic of small doses of dopamine agonists. Both the hypodipsic and sedating effects of ET 495 were completely reversed by pretreatment with spiperone. The slight hypodipsia produced at 20 mg . kg-1 was accompanied by signs of low intensity behavioural stereotypy. The stereotypy, unlike the other behavioural effects of ET 495 treatment, was not antagonized by spiperone pretreatment.

Animals↗
PubMed1982

Caffeine-induced hypodipsia in water-deprived rats: relationships with benzodiazepine mechanisms.

The effects of caffeine (3-100 mg/kg) on water intake and the time course of drinking were investigated in male rats which had been adapted to a daily 22 hr water deprivation schedule. Doses of caffeine were found which significantly depressed water intake, reduced the time to the first interruption in drinking, and depressed the time course of drinking, without manifestly affecting the efficiency of drinking. At the highest dose, however, caffeine had a major suppressant effect on drinking, which was accompanied by signs of motor interference. The hypodipsic effect of caffeine was reversed by benzodiazepine treatment (midazolam or diazepam). However, the convulsant benzodiazepine Ro5-3663 which on electrophysiological evidence can act as a GABA antagonist also reduced drinking, adding to the hypodipsic effect of caffeine. A water load prior to the drinking test produced satiation effects, closely reminiscent of the effects of caffeine at lower doses. The possible mimicry of thirst satiety by caffeine is discussed, together with possible underlying mechanisms of caffeine-benzodiazepine interactions.

Animals↗
PubMed1982

Enhancement of osmotic- and hypovolemic-induced drinking by chlordiazepoxide in rats is blocked by naltrexone.

Recent reports indicate that benzodiazepine-induced hyperphagia can be antagonised by naloxone, an opiate antagonist. Benzodiazepines are also known to facilitate water ingestion in water-deprived rats, and the present study showed that in addition, benzodiazepine treatment can enhance drinking which is elicited by an osmotic thirst stimulus (2 M hypertonic saline) or by a hypovolemic thirst stimulus (20% polyethylene glycol). In both cases, low dose levels of naltrexone (also an opiate antagonist) dose-dependently suppressed the facilitation of thirst-aroused drinking by chlordiazepoxide. Taken with recent biochemical data these behavioral results indicate that the enhancement of ingestive responses by benzodiazepines may depend upon a naloxone-reversible release of endogenous opioid peptides.

Animals↗
PubMed1982

Palatability-induced drinking after administration of morphine, naltrexone and diazepam in the non-deprived rat.

Rats consumed excessive quantities of a highly palatable 0.005M sodium saccharin solution in the absence of depletion of body fluid compartments. The taste strongly promoted drinking, and the consequent fluid consumption proved to be very sensitive to opiate receptor blockade. Naltrexone, at a dose as small as 0.03 mg/kg, significantly attenuated consumption of the saccharin solution in the first hour of access. The naltrexone treatment did not affect latency to drink, and its suppressant effect was transient, indicating that it did not induce either immediate or lasting avoidance of the saccharin solution. The naltrexone-induced suppression was also not due to elicited stress or anxiety, since concurrent administration of diazepam did not reverse the naltrexone effect. Morphine (0.3-3.0 mg/kg) failed to enhance saccharin solution intake over a 6 hr test period. Morphine (10 mg/kg) produced immobility and an extended suppression of drinking, which was followed by a secondary hyperdipsic response.

Animals↗
PubMed1982

Lack of effect of contralateral speech discourse on auditory threshold response behavior.

Three pilot experiments were conducted with normal-hearing adults on the effects of contralateral speech discourse on monaural intensive threshold at 1 kc/s. Two voices simultaneously reading dissimilar passages were presented to the non-test ear. Pure tones and speech were led to insert receivers. Threshold assessment was by operant techniques with feedback for correct response. Stimulus presentation and response recording and retrieval were under computer control. Performance was analyzed by threshold central tendencies and variances, by slopes of performance-level curves, and by slopes of curves for response-decision latencies vs level. In Exper. I (N:5), Ss made threshold judgments while in the contralateral ear speech was presented at 30 db SL, in 2-sec samples with 2-25- sec silent intervals intervening. In Exper. II (N:3), the interrupted speech was at levels of -10, 10, 50, and 70 db; in addition, 4 blocks of thresholds were taken at 30 db SL to examine adaptation effects, if any. In Exper. III (N:3), speech was continuous at the levels of 10, 30, 50, and 70 db. None of the characteristics of the speech appeared to affect performance by any of the 3 indices at any level, for any S systematically. It was concluded that inter- and intra-subject variability may be the key to much of the conflicting results in the literature in the area of performance in noise.

Adaptation, Physiological↗
PubMed1981

Food preference following acute or chronic chlordiazepoxide administration: tolerance to an antineophobic action.

Chlordiazepoxide (CDP) at 15 mg/kg produced two distinct actions in a food preference test, firstly a general appetite-enhancing effect, and secondly an anti-neophobic effect. Following acute injection of CDP the rats changed from eating predominantly familiar food to a novel food. This may signify an anti-neophobic effect of CDP. However, following 10 days of treatment with CDP, the anti-neophobic effect was abolished and the choice of familiar food was enhanced. This could be an indication of a more general appetite-enhancing effect. Hence some form of tolerance may develop to CDP's effects over 10 days of treatment which selectively abolishes anti-neophobic action whilst leaving the appetite effect further enhanced. There were no indications of tolerance developing to the actions of CDP in animals familiarized with all the test foods before the preference test was run. Hence the presence of food novelty may be critical to the observation of some form of selective tolerance.

Animals↗
PubMed1981

Effects of acute or chronic administration of low doses of a dopamine agonist on drinking and locomotor activity in the rat.

Low doses of piribedil (0.25-5.0 mg/kg) administered acutely produced reliable decrements in locomotor activity in thirsty and non-thirsty animals, the greatest effect occurring at the highest dose. A sequence of ten daily injections of piribedil produced indications of the development of tolerance, at the two highest doses (2.5 and 5.0 mg/kg) in thirsty animals. The smallest doses used, given either acutely or chronically, produced a weak enhancement of drinking behaviour within the first 15 min of a drinking test, as shown by a reduction in latency to drink and an increase in the amount of water consumption. Tolerance did develop with respect to drinking behaviour; animals treated chronically with piribedil displayed higher levels of drinking at several dose levels when compared with acutely treated subjects. The tolerance displayed at the two highest doses could have a close affinity with that shown with regard to locomotor activity.

Animals↗
PubMed1981

The effect of fenfluramine on the microstructure of feeding and drinking in the rat.

1. The effects of three doses of fenfluramine on feeding and drinking in the rat were examined. 2. Feeding and drinking were subdivided into meals and bouts, and the changes in feeding/drinking were expressed in terms of meal/bout frequency, meal/bout size, meal/bout length, and eating/drinking rate. 3. The changes in these parameters were examined over different time periods after the injection. 4. Significant changes in the distribution of inter-response intervals within meals were found in time period 1 with 5 mg/kg and 10 mg/kg doses of fenfluramine. Videotape and computer analysis showed that the changes in inter-response interval histograms differed significantly from those seen in normal animals approaching satiety. Drinking parameters also changed. 5. Compensatory increases in feeding were observed in time period 4 with the 10 mg/kg dose. 6. The difficulties in designing and interpreting experiments in feeding are discussed, and the action of fenfluramine as an anorectic drug is considered.

Animals↗
PubMed1981

Propranolol in schizophrenia. I. Comparison of propranolol, chlorpromazine and placebo.

Fifty-three hospitalized chronic schizophrenic patients were treated with either propranolol, chlorpromazine or placebo in a double-blind randomized trials for up to three months. Propranolol in a usual dose of 640 mg/day, produced marked cardiovascular effects but no improvement in schizophrenic symptomatology relative to placebo. The effects of chlorpromazine were small and inconsistent.

Blood Pressure↗
PubMed1980

Effects of chlordiazepoxide and diazepam on feeding performance in a food-preference test.

Chlordiazepoxide (5 and 10 mg/kg) and diazepam (2.5 mg/kg) reduced the latency to eat and enhanced feeding response to familiar food in a food-preference test. The increased feeding response resulted from an increased frequency of individual eating episodes (bouts) without significant change in the episode duration. Experiment II indicated that this facilitatory action of the two drugs was not dependent on the presence of principal novelty cues in the food-preference test. Diazepam (5 mg/kg), in contrast, enhanced the feeding responses to novel food in the food preference test. Experiment III demonstrated that although diazepam can counteract induced food neophobia, its facilitory action on the response to novel foods may be mediated by a mechanism which can operate independently of food neophobia.

Animals↗
PubMed1980

Interactions of chlordiazepoxide and anorectic agents on rate and duration parameters of feeding in the rat.

d-Amphetamine (0.5 and 1.0 mg/kg) and dl-fenfluramine (2.0 and 4.0 mg/kg) reduced food intake in a short exposure feeding test, and their effects were counteraated by chloriazepoxide, particularly at 50 mg/kg. Chloriazepoxide reduced latency to eat, extended the durationof feeding and depressed the rate of feeding. Antagonism occurred in combination with d-amphetamine in relation to latency and duration, but in this experiment d-amphetamine did not affect feeding rate. Antagonism also occurred in combination with fenfluramine, with latency and duration measures, but only at the lower chlordiazepoxide dose. Instead, chlordiazepoxide (10.0 mg/kg) enhanced fenfluramine's effects to reduce feeding duration and feeding rate.

Animals↗
PubMed1980

Naloxone: effects on food and water consumption in the non-deprived and deprived rat.

Naloxone (0.5--5 mg/kg) reduced both food and water intake in non-deprived male rats, tested in the dark phase of the light-dark cycles in their home cages. These effects were transient; food and water-intake were restored to control levels by the end of the 8-h test period. The effects were also not dose-related. Naloxone (1 and 5 mg/kg) also reduced water-intake in water-deprived and food-deprived animals, without altering food-intake. These results suggested that naloxone may exert a primary antidipsogenic action, that does not depend upon any suppression of feeding. A final experiment showed that naloxone can completely abolish the thirst produced by injection of a hypertonic saline solution. This experiment also demonstrated that naloxone could suppress feeding, even though food intake was markedly inhibited by the osmotic thirst stimulus. Hence, the activation of feeding responses (e.g. by food deprivation) is not a necessary condition for naloxone to suppress feeding. The implications of these results for the control of feeding and drinking responses are briefly considered.

Animals↗
PubMed1980

Effects of chlordiazepoxide, food familiarization, and prior shock experience on food choice in rats.

Chlordiazepoxide (5, 10 mg/kg) increased the time devoted to eating familiar laboratory chow without altering the response to a range of novel, palatable foods which were also available to the food-deprived rats. Prior experience with the same range of alternative foods (food familiarization) radically changed the effect of the drug. After familiarization with these foods, chow was virtually ignored as a food choice, indicating its low relative palatability; chlordiazepoxide then prolonged the time eating the familiarized foods without significantly increasing the response to chow. These results are not consistent with an anti-food neophobia action of chordiazepoxide. They suggest instead that chlordiazepoxide enhances feeding responses related to food saliency. Footshock, delivered two days before the food choice test affected performance within the test. Its effects were opposite those of chlordiazepoxide, but they competed additively with the drug's effects. These results indicate that chlordiazepoxide's action was not simply to remove any inhibitory effect on feeding produced by fear; instead the drug promoted approach to food antagonizing any deficit in approach associated with fear. These findings are viewed as consistent with an action of chlordiazepoxide to augment the level of feeding motivation. Chlordiazepoxide (15 mg/kg) may act to overcome food neophobia.

Animals↗