Rats with bilateral lesions of lateral entorhinal cortex and perirhinal cortex were tested on a nonrecurring-items delayed nonmatching-to-sample (DNMS) task resembling the one that is commonly used to study object recognition in monkeys. The rats were tested at retention delays of 4 s, 15 s, 60 s, 120 s, and 600 s before and after surgery. After surgery, they displayed a delay-dependent deficit: They performed normally at the 4-s delay but were impaired at delays of 15 s or longer. The addition of bilateral amygdala lesions did not increase their DNMS deficits. The present finding of a severe DNMS deficit following rhinal cortex damage is consistent with the authors' previous finding that bilateral lesions of the hippocampus and amygdala cause only mild DNMS deficits in rats unless there is also damage to rhinal cortex (D.G. Mumby, E.R. Wood, & J.P.J. Pinel, 1992). These findings add to accumulating evidence that the rhinal cortex, but not the amygdala, plays a critical role in object recognition.
In typical laboratory settings, the defensive reactions of animals appear to be limited tofreezing, fleeing, and attacking. However, in the present investigations, rats.tested in the presence of movable ma-> terial incorporated it into a striking and adaptive behavioural sequence. Rats shocked once through a stationary prod buried this shock ^source, even when the shocks-test interval was 20 days. This burying behaviour occurred at a variety of shock intensities and seemed to be controlled sp cifically by the relation between the shock and the prod; rats shocked through a grid did not bury the prod, and rats shocked by one of two identical prods buried only the shock-prod. Both the position and bright ness of the prod seemed to control the burying behaviour. When either of these cues was changed prior to the test, burying behaviour was disrupted compared to control conditions in which these cues were unaltered. Although burying was a directed and consistent response of rats to prod shock, it was not a simple, reflexive behaviour; rats could adapt their burying behaviour to changes in both the kind and disposition of burying materials. Thus, the usual assumption that the rat's defensive reper^toire is limited to a few simple behaviours appears to have been shaped by the constraints of standard testing environments rather than by the actual propensities of the rat. These results were discussed in terms of their implications for a "biological" approach to aversive learning.
Behavioral paradigms that have been designed to mimic forms of learning that are important for the survival of animals in the wild, rather than to minimize the contributions of adaptive predispositions, may prove to be particularly useful for studying the behavioral effects of drugs. In the present experiments, the propensity of rats to bury sources of aversive stimulation was disrupted in a dose-dependent fashion by a single injection of the anxiolytic drug, diazepam. This suggested that the conditioned defensive burying paradigm could prove to be a valuable addition to the paradigms available for studying anxiolytic effects. Supporting this view were two additional observations. First, the relative potencies of diazepam, chlordiazepoxide, and pentobarbital in the burying paradigm compared favorably with their relative potencies in clinical settings. Second, the effects of anxiolytics on conditioned burying appeared to be dissociable from the effects of other drugs that disrupt this behavior.
Humans and other warm-blooded animals living with continuous access to a variety of good-tasting foods tend to eat too much and suffer ill health as a result--a finding that is incompatible with the widely held view that hunger and eating are compensatory processes that function to maintain the body's energy resources at a set point. The authors argue that because of the scarcity and unpredictability of food in nature, humans and other animals have evolved to eat to their physiological limits when food is readily available, so that excess energy can be stored in the body as a buffer against future food shortages. The discrepancy between the environment in which the hunger and eating system evolved and the food-replete environments in which many people now live has led to the current problem of overconsumption existing in many countries. This evolutionary perspective has implications for understanding the etiology of anorexia nervosa.
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