Neil Rowland

Morphine antagonists and consummatory behaviors

Opiate antagonists were tested for their effects upon either drinking or eating in eight experiments. Naloxone, nalorphine, and the active isomer of WIN 44,441 all reduce drinking. Neither an analog of nalorphine that does not cross the blood-brain barrier, nor the inactive isomer of WIN 44,441 is effective in reducing water intake. These data provide support for the conclusion that these antagonists ahve stereospecific effects within the central nervous system. Naloxone suppresses drinking following procedures inducing osmotic, volemic, or hormonal thirst. Naloxone suppresses eating following procedures inducing glucoprivation but does not alter eating elicited by tail-pressure. Collectively, these data lead to the conclusion that endorphins play a role in the organization of ingestive behavior following challenges to homeostasis.

Peripherally administered serotonin decreases food intake in rats

We report that intraperitoneal injection of serotonin produces a dose-related decrease in the food intake of hungry rats. The efficacy of serotonin was increased by prior treatment with clorgyline, a type A monoamine oxidase inhibitor. Doses of serotonin which were anorectic did not significantly impair locomotor activity or sensorimotor performance. Further, 2 mg/kg serotonin (ED50 on food intake) did not produce a conditioned taste aversion when paired repeatedly with sucrose ingestion. We conclude that the anorectic effects of serotonin are not secondary to nonspecific effects of the agent, and suggest that peripheral serotonin may play a role in normal satiation.

Effects of insulin and 2-deoxy-D-glucose on feeding in hamsters and gerbils☆

Abstract Golden hamsters ( Mesocricetus auratus ) and gerbils ( Meriones unguiculatus ) increased their food intake and rate of weight gain during daily injections of protamine zinc insulin. Both species showed modest and delayed increases of food intake after acute insulin injections, despite severe hypoglycemia. Neither species increased its feeding after 2-deoxy-D-glucose. The findings are discussed in terms of the relevance of glucoprivation to normal feeding, and possible hormonal abnormalities in hamsters.

Hypothalamic hyperphagia prevented by prior subdiaphragmatic vagotomy: Insulin hyperphagia is unaffected ☆

Abstract Male rats were given bilateral subdiaphragmatic vagotomy or a sham operation. Both groups of animals showed equivalent hyperphagia and weight gain during a ten day treatment with long-acting insulin. Despite this ability to increase feeding, the vagotomized rats did not overeat and become obese after VMH lesions.

Regulatory drinking: Do the physiological substrates have an ecological niche?☆

Abstract The current physiological theories of thirst are briefly reviewed, and a number of experiments in which drinking behavior does not conform to such models are described. These include parenteral self-administration and taste adulteration experiments. Regulatory drinking may be identified in these preparations, but is substantially different from that defined by simple physiological models. Similarly aberrant regulatory drinking is seen after a variety of hypothalamic lesions, and the interpretation of such experiments is discussed. Finally, the relevance of some laboratory paradigms to the normal (ethologically determined) controls of drinking is questioned, and it is suggested such factors should be incorporated into future models.

Comparison of the suppression by naloxone of water intake induced in rats by hyperosmolarity, hypovolemia, and angiotensin

The effect of naloxone upon water consumption by rats was assessed using two intensities each of IV NaCl (Hyperosmolarity), SC polyethylene glycol (hypovolemia), and IV angiotensin II. In each case naloxone produced a dose-related reduction in the amount drunk. Angiotensin-induced drinking was most easily inhibited, and was abolished by only 1 mg/kg naloxone. In contrast, 1 mg/kg naloxone produced only a 50% reduction NaCl-induced drinking, and hypovolemia-induced drinking was not completely reversed by 5 mg/kg. Naloxone was without effect upon the natriuresis after NaCl, or the hypertension during AII administrations. Parallels are drawn between the effects of naloxone on these types of thirst, and of other perturbations including brain damage and taste adulteration.

Differential effects of glucose and fructose infusions on insulin-induced feeding in rats ☆

Abstract Intravenous administration of large doses of insulin rapidly lowered blood glucose concentration and elicited feeding behavior in rats. Infusion of glucose solution into the jugular vein suppressed the feeding response on a calorie-for-calorie basis. Infusion of fructose, a hexose that can nourish peripheral tissue but cannot be oxidized by brain, also lowered food intake after insulin treatment despite continued hypoglycemia. However, the effects of fructose were not as great as those of equimolar glucose solutions except when relatively small doses of insulin were given. These results provide further evidence that a peripheral factor, perhaps involving the liver, can attentuate the feeding that is initiated by acute glucoprivation.

Hypotension and thirst in rats after isoproterenol treatment

Abstract Drinking induced in rats by systemic isoproterenol treatment is markedly attenuated after bilateral nephrectomy. The present experiments demonstrate that the hypotension produced by iso-proterenol treatment was more profound, and lasted much longer, in nephrectomized rats than in intact animals. When arterial blood pressure was partially elevated by central administration of angiotensin II or carbachol (Experiment 1) or by intraarterial infusion of epinephrine (Experiment 2), drinking behavior was restored in the nephrectomized animals and their water intakes approximated the amounts consumed by intact rats given isoproterenol. In general, an inverted U-shaped curve was found to define the relation between blood pressure and water intake in rats after isoproterenol treatment. Drinking was most probable when mean arterial blood pressures were in the range of 70–85 mm Hg, whereas rats were unlikely to drink when blood pressures were much below or above this range. These findings indicate that isoproterenol-induced thirst is not dependent on a renal dipsogen, and suggest instead that the hypersecretion of renin that occurs in intact rats is simply permissive of drinking behavior by modulating the hypotensive effects of the drug treatment.

Hypothalamic hyperphagia prevented by damage to brain dopamine-containing neurons.

Abstract Bilateral damage to the ventromedial hypothalamic region in otherwise intact rats produced hyperphagia and weight gain. Rats which had incurred extensive damage to ascending dopamine-containing pathways as a result of intracerebral 6-hydroxydopamine injections failed to overeat or to gain excessive weight following ventromedial hypothalamic damage. They were, however, hyperactive and hyperemotional shortly after this lesion. We suggest that the integrity of the ascending dopaminergic fibers is critical for the appearance of the hypothalamic hyperphagia syndrome.

Feeding and drinking interactions after acute butyrophenone administration

The effects on feeding and drinking of various doses of droperidol, haloperidol and spiroperidol were studied in a number of paradigms. All three buryrophenones produced generally similar effects. After food deprivation, feeding was slightly increased at low doses but was decreased at the higher doses; the concomitant postprandial drinking was attenuated at all doses. Desalivate rats showed a marked attenuation of feeding (and prandial drinking) at low doses, but when wet mash was given instead of pellets and water a normal dose-response relationship was obtained. After water deprivation drinking was attenuated at all doses, and when food was also available during the drinking test the food intake was decreased in proportion to the drinking. Drinking was blocked more when food was present than in its absence. Insulin and 2-deoxyglucose induced feeding in sated rats was attenuated but not abolished by haloperidol. The findings are discussed relative to the role of activation and brain catecholamines in feeding and drinking.