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Biomedical subjects

N Rowland

Publications and source records attributed to N Rowland.

At least 55 records · Page 3Linked to original sources
PubMed1981

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.

Animals↗
PubMed1981

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.

Angiotensin II↗
PubMed1981

Impaired drinking responses of rats with lesions on the subfornical organ.

electrolytic lesions of the subfornical organ (SFO) in rats are known to abolish their drinking response to intravenous infusion of angiotensin II (AII). Such lesions also attenuate drinking after 20% polyethylene glycol solution (PEG) is given subcutaneously, which suggests that AII may play an important role in mediating thirst during hypovolemia. However, the present studies show that such rats with SFO lesions may drink normal amounts when larger plasma volume deficits are caused by 30% PEG treatment. They also may drink normal amounts in response to 20% PEG when pretreated either with caffeine or hypertonic NaCl solution. Furthermore, they may not drink in response to relatively low doses of hypertonic saline but drink normal amounts when given larger doses. These and other results suggest that the SFO is involved in a control system for thirst and that after damage to it, greater stimulation than usual may be required for drinking to be initiated. From this perspective, drinking would be expected following either suprathreshold stimulation or drug-induced lowering of the activation threshold in these animals, as was observed, with the loss of putative AII receptors in the SFO also contributing to their particularly severe deficits in thirst induced by AII.

Angiotensin II↗
PubMed1980

Orbital or medial frontal cortical lesions have different effects on tail pressure-elicited oral behaviors in rats.

Three groups of rats were tested with daily tail pressure (TP) tests until reliable and stable baseline eating, gnawing or licking was observed. One group then received bilateral aspiration of the medial frontal cortex, a second group received orbital frontal cortical lesions, and a third group received control lesions of the motor cortex. Daily TP tests were continued postoperatively. There was no disruption of TP-elicited oral behaviors after medial frontal or motro cortex lesions. In contrast, orbital frontal lesions abolished TP behaviors on the first day postoperatively, and there was a slow recovery of TP until day 5 when the elicited behaviors were about 80% of preoperative levels. The time course of recovery of TP-elicited oral behavior closely paralleled the recovery of elective eating after orbital frontal lesions, both in the group given TP and in another group given orbital lesions but not TP. These data demonstrate a marked difference between the medial and orbital divisions of the prefrontal cortex in the mediation of stress-induced oral behavior, and we discuss our data in terms of the possible role of dopamine terminals in these regions.

Animals↗
PubMed1980

Impaired drinking to angiotensin II after subdiaphragmatic vagotomy in rats.

Rats received total bilateral subdiaphragmatic vagotomy and, one month later, were fitted with chronic intravenous or intracerebroventricular cannulas. The vagotomized rats showed much reduced drinking compared with controls during intravenous infusion of angiotensin II. Their drinking to intracerebroventricularly administered angiotensin II was, however, less affected. The possible role of the vagus nerve in the mediation of angiotensin and other types of drinking is discussed.

Angiotensin II↗
PubMed1979

Physiological and behavioral responses to starvation in the golden hamster.

Physiological and behavioral responses of adult hamsters to starvation were studied by measuring food intake, weight recovery, serum concentrations of glucose, insulin, free fatty acids and beta-hydroxybutyrate, and ketonuria in animals subjected to different weight losses, diets, and durations of fast. Hamsters were debilitated by fasts longer than 12 h or leading to greater than 20% weight loss. Hamsters' feeding patterns were unmodified by fasts ranging between 5 and 12 h and showed no circadian periodicity. Hamsters predominantly recovered from weight losses without increasing their food consumption (unless they were offered a diet of pellets and seeds) and without changing their meal patterns, at a rate of weight gain proportional to the magnitude of preceding weight loss if provided with uninterrupted access to food. By 8 h of fast, blood metabolites were indicative of mobilization of body fat. Hamsters are thus behaviorally unresponsive to duration of fast, but compensate physiologically for weight losses with proportional increases in the rate of weight gain.

Animals↗