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Biomedical subjects

L Devenport

Publications and source records attributed to L Devenport.

8 recordsLinked to original sources
PubMed1992

Mimicking corticosterone's daily rhythm with specific receptor agonists: effects on food, water, and sodium intake.

The endogenous pattern of type I and II corticosteroid receptor stimulation was systematically assembled from specific agonists in order to detect any unique receptor interactions in the control of ingestive behavior. The type II agonists dexamethasone (0, 5, or 25 micrograms/kg) or RU28362 (0, 5, or 25 micrograms/kg) were injected daily in the final hour of the light phase of the illumination cycle of adrenalectomized rats. This was carried out in the presence or absence of continuous aldosterone (type I agonist) infusion. Additional comparisons were made with sham-operated groups and animals receiving type II agonists by continuous infusion. Type II agonists increased the intake of 2% saline and the proportion of food taken at night, but had negligible effects on total food intake. Type II agonists did not interact with the type I agonist. Type II effects were greatly potentiated by continuous infusion, though administered at the same doses as acute injection. When the effects of type II receptor stimulation emerged, they always consisted of an exacerbation of the adrenalectomy syndrome, not a return to normal quantities or patterns. In contrast, type I receptor stimulation restored both the quantities and unique day-night patterns of saline, water, and food intake to values matching intact animals. The findings suggest that the behavioral significance of corticosterone's nocturnal peak of type II stimulation is small, and that its most important function may lie in the metabolic processes it instigates during its steady rise in the light phase.

Adrenalectomy↗
PubMed1992

The relationship between adrenal steroids and enrichment-induced brain growth.

The question of whether brain growth brought about by environmental enrichment is mediated by the adrenal cortex has not been answered. Accordingly, young male rats were either adrenalectomized (ADX) and infused with a constant maintenance dose of corticosterone (2 mg.kg-1.day-1) or sham-operated and implanted with a blank infusion device. Half of each surgical group was maintained in either impoverished (IC) or enriched conditions (EC). After 30 days, changes in forebrain growth and thickness of various cortical and subcortical regions were determined for each group. Enrichment and ADX independently increased forebrain weight and thickened cortical tissue at about the same anatomical sites. However, combined treatments were additive, not interactive. EC-induced brain growth is mimicked but not mediated by adrenalectomy.

Adrenal Glands↗
PubMed1991

Macronutrient intake and utilization by rats: interactions with type I adrenocorticoid receptor stimulation.

Corticosterone-free (adrenalectomized, ADX) and intact rats were offered experimentally compounded diets in which 65% of available calories were supplied by a single macronutrient (single-diet study). ADX impaired the intake, weight gain (especially as body fat), and efficient utilization of high-protein and high-fat diets. In contrast, no behavioral, metabolic, or compositional changes could be found among ADX rats maintained on a diet high in carbohydrates. When ADX rats were given separate sources of macronutrients (self-selection study) they did not self-select a high-carbohydrate diet. Instead, they displayed a strong fat avoidance and a relative increase in protein intake, the macronutrient they utilize least efficiently. Separate groups of ADX animals were continuously infused with 25 or 125 micrograms.kg-1.day-1 aldosterone, a specific type I adrenocorticoid receptor agonist. Type I receptor stimulation eliminated all ADX-related deficiencies found in the single-diet and self-selection studies: caloric intake, feeding efficiency, carcass composition, and macronutrient preferences were restored to or beyond the corresponding values of adrenal-intact rats. The normal rat's ability to ingest and utilize macronutrients optimally is dependent on corticosterone's stimulation of type I receptors.

Adrenal Glands↗
PubMed1990

Acute, chronic, and interactive effects of type I and II corticosteroid receptor stimulation on feeding and weight gain.

Type I (aldosterone) and/or type II (dexamethasone or RU28362) corticosterone receptor agonists were continuously infused in adrenalectomized Sprague-Dawley rats for 28 days at doses of 3.4, 17.2, or 86.2 nmol/day. Additional groups received combined agonist infusions, blank infusions, or sham operations. The type I agonist stimulated body weight gain, and the type II agonists were both suppressive, differing mainly in degree. Although there were a few early effects of these hormones (usually a stage of exaggerated activity), once passed, chronic stimulation was marked by steady or slightly increasing steroid influence on body weight. Throughout the chronic phase of this study there was no departure from a simple opponent model of type I and II ligand actions, and their combination approximated an arithmetic summation of the two separate agonists. This was generally true of feeding as well, although steroid effects on intake were always less pronounced. In contrast to chronic administration, acute combinations of these agonists were highly interactive, producing slight losses than large gains for the aldosterone and RU28362 combinations, but a large gain then small loss for the aldosterone and dexamethasone combination. These results imply that RU28362 and dexamethasone differ in more respects than potency. Because normal endogenous type II stimulation is acute and occurs against a background of type I receptor occupation, mixed agonist interactions are probably the rule for everyday physiological activity, not the exception.

Aldosterone↗
PubMed1989

Corticosterone's dual metabolic actions.

Corticosterone possesses two distinctly opposite metabolic actions. The actions are strictly dose-dependent and are linked to type I and type II corticosteroid receptor binding. These conclusions are drawn from continuous infusion studies where corticosterone yields a bitonic dose-response curve for body weight gain and feeding efficiency. Anabolic at low serum levels, corticosterone concentrations above 2 micrograms/dl bring about an opponent catabolic process that intensifies and eventually masks the anabolic action. Relatively pure type I (aldosterone) and type II (RU28362 and dexamethasone) corticosterone receptor agonists produce opposite monotonic functions that respectively mimic the ascending and descending arms of the corticosterone dose-response curve. Stimulation of either receptor increases the proportion of carcass fat to lean body mass by either increasing carcass lipids (type I) or by reducing protein (type II).

Aldosterone↗
PubMed1989

Ethanol and spatial localization.

Water (Exp. 1) and radial maze (Exp. 2) tasks permitted an evaluation of the relative degree of impairment imposed by ethanol (0, 0.75, 1.5, and 2.0 g/kg) on cognitive mapping vs. cued place learning. The tasks did not require working memory. A strong tendency emerged for ethanol-treated rats to persist in cognitive mapping strategies after the strategies were no longer useful, but there was no indication of a mapping impairment per se. When performance deficits appeared, they were equivalent across mapping and cued place tasks and may have reflected motivational effects of ethanol. In most instances, neither mapping nor cued place tasks were difficult for ethanol-treated animals unless the tasks required abandoning one strategy for another. The tenacity of ethanol-treated rats to use cognitive mapping strategies, particularly rats receiving the highest dose, proved consistent and theoretically decisive. The behavioral invariance of ethanol-treated rats is not caused by a cognitive mapping deficit. Rather, mapping is another domain in which ethanol reduces flexibility.

Animals↗
PubMed1987

Aldosterone and the mobilization of energy.

Aldosterone diminishes the ability to endure starvation. Its exogenous administration to adrenalectomized rats advances the onset of hypothermia and death. The impairment seems to lie in an inability to mobilize energy stores fully: animals given the steroid are unable to lose weight at a normal rate. The findings help to establish the significance of mineralocorticoids in the regulation of energy exchange and solve some theoretical questions as to their general mode of action.

Adrenalectomy↗