The role of urine marking in the foraging behaviour of least chipmunks.

Least chipmunks Tamias minimus, occasionally deposit urine on buried patches of seeds after sampling the patch, a behaviour never before reported for rodents. The results of these experiments show that (1) patch-marking is a deliberate act, bearing no resemblance to routine excretion, (2) marking deters both the marker and conspecifics from harvesting attempts, (3) chipmunks can discriminate their own marks from those of others, and (4) the incidence of marking in the wild is at least as frequent, and its deterrent effect as strong as in the laboratory. Although the message conveyed by a mark is clearly exploited by conspecifics, and may benefit kin, the results accord best with prevailing theory advanced for canids, that an olfactory reminder of patch value improves the marker's foraging efficiency. Copyright 1999 The Association for the Study of Animal Behaviour.

Future value and patch choice in least chipmunks.

Animals subsisting on non-renewing patches confront a unique valuation problem, in which the objective value of a patch is inversely related to the amount already harvested. We investigated whether the subjective patch valuations of captive least chipmunks, Tamias minimus, reflected this environmental constraint as they foraged for buried patches of seeds. On the day following partial depletion of two patches, chipmunks spontaneously selected the least depleted patch, despite having no direct information about its former or present value. These findings held across experiments in which the order and extent of patch depletion were under the forager's control or experimental control. The animals consistently chose sites from which they had taken the fewest items, despite experiencing no difference in relative capture rate, suggesting that they discounted patch value on the basis of amount harvested or harvest time. Furthermore, the animals refused to return to patches they had completely depleted, and when induced to re-dig depleted patches by placing seeds above them, the animals chose randomly despite a three-fold difference in the number of items previously taken from each, suggesting that they disregarded rewards taken, attending only to the amount remaining. Subsequent experiments showed that chipmunks can take past reward history into account. When we refilled previously depleted patches and induced chipmunks to re-dig and deplete them again, they treated the patches as renewable types and represented their value in terms of the amount removed, not the amount left. Thus, the assessment mechanism of least chipmunks is facultative: they expect that patches will not replenish, but are prepared for exceptions. Copyright 1998 The Association for the Study of Animal Behaviour. Copyright 1998 The Association for the Study of Animal Behaviour.

Relative contribution of type I and II corticosterone receptors in VMH lesion-induced obesity and hyperinsulinemia.

Ventromedial hypothalamic (VMH) lesion-induced obesity is accompanied by hyperinsulinemia and hyperphagia, which are dependent upon corticosterone (Cort) for their expression. Whether Cort exerts these actions through its stimulation of type I or II Cort receptor populations is unknown. Therefore, food intake and weight gain were measured in obese adrenalectomized VMH-lesioned rats given continuous infusion of various doses of either a type I-receptor agonist (aldosterone), a type II-receptor agonist (RU-28362), or several combination doses. Similarly, the receptor population responsible for lesion-induced hyperinsulinemia was identified. Type II receptor stimulation restored the hyperphagia, weight gain, and hyperinsulinemia of adrenalectomized VMH-lesioned animals, while type I receptor stimulation blocked their weight loss.

Time-dependent decisions in dogs (Canis familiaris).

We investigated whether the foraging decisions of dogs (Canis familiaris) were time dependent and consistent with a temporal weighting rule (TWR) for maximizing the reliability of information. Dogs were given information about patches whose qualities varied over time. To simulate natural conditions, we interposed interruptions at selected points in foraging. Patch choices were time dependent and closely matched the predictions of TWR. Dogs relied on very recent information when available, but with increasing delays they used patch averages. TWR may be a general solution to problems faced by foragers in variable environments.

Exercise endurance in rats: roles of type I and II corticosteroid receptors.

Intact and adrenalectomized (ADX) rats were mildly food deprived and administered dexamethasone (type II agonist), aldosterone (type I agonist), corticosterone (mixed agonist), or vehicle 24 and 2 h prior to forced exercise in a treadmill. The endurance of intact animals was unaffected by hormone treatments. Adrenalectomy greatly advanced the onset of fatigue, and aldosterone exacerbated the effect of adrenalectomy. Corticosterone improved endurance in ADX rats, and dexamethasone was even more potent in this respect. Aldosterone slowed deprivation-induced weight loss in ADXs, while corticosterone and especially dexamethasone accelerated loss. Thus, endurance was directly related to body weight loss, and presumably to the fuels released by such loss. The results extend the type I-type II functional dichotomy to the delivery of utilizable energy for metabolically active tissues.

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.

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.

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.

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.

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.

Contributions of hippocampus and neocortex to the expression of ethanol effects.

The distinctive effects of ethanol on behavior suggest that certain parts of the CNS may be especially sensitive to it. One of the primary candidates is the hippocampal formation. Damage to this structure mimics acute ethanol treatment across a wide variety of behavioral tasks and processes. The possibility of a hippocampal basis for ethanol psychopharmacology was examined in the present experiments. Chosen for behavioral analysis were relatively complex eight-arm radial maze tasks which have independently been shown to be sensitive to ethanol administration and hippocampal lesions. Measures included arm selection predictability, vigilance, and retardation of extinction. Bilateral hippocampal lesions or ethanol injection (1.5 g/kg, IP) produced similar effects. However, hippocampectomy did not disrupt ethanol's influence on any task. Comparatively, neocortical ablation, especially prefrontal, was quite effective in this respect. It blocked or reduced two of the drug's three behavioral effects examined here, without any strong influence of its own, and without altering blood alcohol concentration.

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).

Site specificity of adrenalectomy-induced brain growth.

Infant, juvenile, and adult brain growth is modulated by corticosterone. This study was designed to determine whether such modulation is confined to certain specific brain areas, and if the pattern of growth revealed is consistent across strains of rats. Young female Sprague-Dawley-derived rats were either adrenalectomized (ADX) or sham-operated (Sham) and allowed to mature 45 days before they were sacrificed for histological analysis. Fore brain sections were taken at several planes for display by projection microscope. Of the 21 sites examined, ADX exerted its greatest effect upon neocortical tissue and myelinated fiber tracts. The only other brain region affected was thalamus, which exhibited a significant widening as a result of ADX. In contrast, archicortical structures were notably unaffected by ADX. Neither the hippocampus, measured from a variety of planes, nor nuclei in the septal area were subject to increased growth by ADX. This general portrayal of ADX's site specificity held across strains of rats. However, there were local differences. Within the neopallium, the frontal region underwent the greatest thickening in one strain, while the occipital area was most strongly affected in the other. Parietal cortex was equally responsive in both strains. The pattern of sensitive vs insensitive sites bore a resemblance to the pattern of increased growth brought about by environmental enrichment as well as the fore brain distribution of Type 2 corticosterone receptors.

Sampling behavior in the radial maze and operant chamber: role of the hippocampus and prefrontal area.

Rats were observed in the radial maze and in an operant setting where "errors" were, within limits, impossible to commit. Under these circumstances, the animals were free to seek information from the environment by varying their behavior, if they chose to do so, without penalty of nonreward. Rats with hippocampal, but not prefrontal or parietal damage, sampled fewer successive arm choices in the maze and exhibited a greatly reduced sensory analysis of the maze and its context. In operant chambers equipped with multiple levers, only hippocampal lesion narrowed the variety of interresponse intervals, which resulted in rhythmic responding. In contrast, the distribution of responses across the three response targets was not influenced by central nervous system injury. This pattern of information deprivation imposed by the hippocampal lesion parallels the profile of performance of such animals on more conventional tasks that depend on such information for optimal performance. Importantly, the sampling deficits were not direct outcomes of the hippocampal damage. Close scrutiny revealed that the rigidity developed over time, albeit quite rapidly. Thus the narrowed behavioral variation following hippocampectomy depends on some interactive component of task experience. We argue that reward is the other critical ingredient.

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.

Environmental control of energy metabolism in rats.

Food availability was arranged so that episodes of feeding were separated by long periods of deprivation. Distinctly different contexts were associated with each condition. For other animals, relatively short periods of deprivation stood in contrast to relatively long opportunities to free-feed, and were also embedded in widely differing physical contexts. These temporal relationships among the conditions were adjusted to sharpen the saliency of each metabolic condition and thereby enhance its associability with the distinctive environment in which each occurred. To avoid the possibility of circadian entrainment, the feeding or deprivation episodes occurred at unpredictable times according to a variable-time schedule. Following several training cycles and an extended period of free-feeding in a neutral environment, the animals were reexposed to the various contexts and sacrificed for metabolite assays. The environment predictive of feeding elevated adipocyte lipoprotein lipase activity and lowered the levels of serum free fatty acids. The deprivation context boosted serum triglycerides and blood urea nitrogen. The conditioned responses were all of a compensatory nature: Feeding cues resulted in accelerated caloric deposition, deprivation cues elicited conditioned mobilization of stored energy. While protein catabolism and several indices of fat metabolism appear to be conditionable, no evidence of environmental control of glycemic responses was observed.

Neonatal aldosterone administration alters later response to adrenalectomy and aldosterone infusion in the rat.

Juvenile and adult infusions of mineralocorticoids promote weight gains in rats. However, nothing is known about the effects of very early administration. As such treatments often bring about enduring changes, we examined the impact of neonatal (days 1-5 of life), followed by early adult (days 45-57 of life), administration of aldosterone (ALDO) on the weight gains of free-fed rats. Analysis revealed that neonatal ALDO exposure altered the pattern of weight gain during the later period. Specifically, acute neonatal exposure increased weight gain in adrenalectomized young adult rats. At the same time, it appeared to reduce the effects of chronic ALDO exposure in these animals.

Ethanol blockade of context change effects.

Rats were trained to run to four baited arms of an eight-arm radial maze. Half the subjects were trained in one context, half in another. Additionally, half of each of these groups received alcohol (1.5 g/kg ethanol) pretreatment while the rest were given saline. Following attainment of criterion, the context conditions were reversed for all subjects, but the drug assignment remained in force. Saline-injected rats were strongly disrupted by the train-test context shift. Alcohol-injected subjects were unaffected by the change in setting. Alcohol seems either to diminish the contextual composition of memories or to block the reaction to environmental mismatch during testing.

Adrenocortical hormones and brain growth: reversibility and differential sensitivity during development.

The brain growth that follows adrenalectomy can be arrested by corticosterone replacement. Administered daily in combination with deoxycorticosterone, the brain and body conditions of intact rats are closely matched. Using this combination dose (corticosterone, 7.0 mg/kg; deoxycorticosterone, 1.0 mg/kg), hormonal replacement was systematically administered and withheld in a balanced design in order to assess the relative sensitivity of brain tissue to corticosteroids across time, and to determine if brain growth suppressed during one phase could recover upon hormone withdrawal during a second phase. Female forebrains were less sensitive to the hormones during an early phase which spanned ages 27 to 46 days. In contrast, 70 to 80% of potential growth was suppressed by replacement during a later period (ages 46 to 65 days). Brain size differences included weight and forebrain length, width, and depth. Hind brains were more sensitive to hormone replacement during phase 1. However, this suppressed growth was completely regained after hormone withdrawal during phase 2. On the other hand, growth that had occurred in the absence of adrenal steroids was not reversed, only arrested, by subsequent administration. We conclude that the rat brain became increasingly sensitive to the suppressive influence of adrenal steroids as females matured from juveniles to adults. Coupled with this sensitivity was the ability--apparently complete--to recover from steroid-induced brain growth suppression.

Effects of alcohol ingestion on zinc content of human and rat central nervous systems.

The abundance of zinc in hippocampal mossy fibers has stimulated investigation of zinc status in various pathologic states in which behavioral or anatomic deficits involving the hippocampus are known to occur. Limited autopsy studies of chronic alcoholic humans have suggested that the content of zinc might be reduced in several brain regions whereas reported attempts to replicate these findings in ethanol-exposed experimental animals have produced inconsistent results. In this comparative study, the zinc concentration in 10 brain regions, all spinal cord segments, and microdissected hippocampal subfields was measured by isotope ratio mass spectrometry. A widespread 15 to 20% reduction in zinc content was observed in all regions of chronic alcoholics compared with controls but a selective involvement of hippocampus was not detected. In the experimental studies, groups of rats were exposed to ethanol by one of three routes: inhalation for 2 weeks, as an ethanol/liquid diet for 3 months, or a single intoxicating i.p. dose. Determinations of tissue uptake of radiozinc and of total zinc content were made. In contrast to human pathologic material, zinc pool size and tissue uptakes were not affected by experimental ethanol administration by any route. This study confirmed that a reduction in zinc concentration occurs in the central nervous system of chronic alcoholics. The animal studies indicated, however, that simple ethanol exposure, even for prolonged periods, does not perturb zinc metabolism in brain. Together, these observations argue that the abnormalities of zinc metabolism in chronic alcoholics are possibly secondary to homeostatic alterations associated with hepatic failure.