The effects of pretraining on the bar-pressing performance of VMH-lesioned rats

King, Bruce M.; Gaston, Michael G.

doi:10.1016/0031-9384(73)90345-4

Cited by 29 publications

(6 citation statements)

References 20 publications

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“…Even more generally, a comparison of the experiments that have measured FR performance of pretrained (Beatty, 1973;Hamilton & Brobeck, 1964; and untrained VMH-lesioned animals (Greenwood etal, 1974;Teitelbaum, 1957) indicates that pretrained animals consistently work for leaner FR schedules than do those without pretraining. Also, experiments that have systematically measured the effect of training on the VMH syndrome have consistently found that pretrained animals exhibit stronger operant performance than do animals with no prelesion training (Beatty, Vilberg, Shirk, & Siders, 1975;King & Gaston, 1973.…”

Section: Food Intake In Operant Tasksmentioning

confidence: 99%

The ventromedial hypothalamic syndrome, satiety, and a cephalic phase hypothesis.

Powley¹

1977

Psychological Review

448

197

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A critical review of the literature on the ventromedial hypothalamic (VMH) syndrome suggests several problems with the available explanations. In particular, explanations of finickiness and hyperphagia fail to account for essential metabolic changes and obesity that occur even when food intake is controlled. Alternatively, hypotheses that offer an account of essential metabolic changes and obesity are unable to explain finickiness satisfactorily. Some mechanism that directly couples sensory events to metabolic responses is apparently responsible for elements of the syndrome. Based on the review, a hypothesis that can account for the finickiness, hyperphagia, and obesity seen in the VMH syndrome is formulated. This hypothesis suggests that VMH lesions produce their major effects on feeding behavior by directly heightening the phasic autonomic and endocrine responses triggered by oropharyngeal contact with food stimuli-the cephalic reflexes of digestion. This proposal can account for finickiness, explain the paradoxes associated with the operant behavior of the lesioned animal, and elucidate the reasons food-restricted VMH animals still fatten. As a working hypothesis, it is parsimonious, empirically testable, and consistent with physiological observations on the VMH syndrome.The feeding disturbances associated with hypothalamic lesions are major models for the physiological analysis of "drive," "motivation," or "emotion." The ventromedial hypothalamic (VMH) synodrome, characterized by dramatic finickiness, hyperphagia, and obesity, is the most completely studied of these models. One reason for the experimental interest in the VMH syndrome is that it evidences a paradoxical dissociation of "hunger" and "food intake" (Miller,

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Section: Food Intake In Operant Tasksmentioning

confidence: 99%

The ventromedial hypothalamic syndrome, satiety, and a cephalic phase hypothesis.

Powley¹

1977

Psychological Review

448

197

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“…Earlier studies showed that large LH lesions resulted in a total loss of sodium appetite in inexperienced rats (Wolf, 1964, Wolf & Quartermain, 1967. Since preoperative test experience can secure for the subject normal or nearly normal performance in a variety of alimentary behaviors after normally disruptive hypothalamic damage (King & Gaston, 1973;Schwartz & Teitelbaum, 1974;Singh, 1973Singh, , 1974, we wanted to determine whether rats with lesions in the LH that were given preoperative experience of saline ingestion and sodium need would show a sodium appetite when tested postoperatively. In contrast to earlier studies, we made small lesions confined to the central region of the LH.…”

mentioning

confidence: 99%

Preoperative sodium experience and hypothalamic lesions in rats.

Ruger¹,

Schulkin²

1980

Journal of Comparative and Physiological Psychology

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When a sodium deficit is induced in rats without lesions, they increase their saline intake regardless of prior experience. By contrast, this experiment found that rats with lateral hypothalamic lesions increased their saline intake only when they had had preoperative experience ingesting saline in response to a sodium deficit. Rats were given natriuretic and mineralocorticoid treatments to induce sodium appetite. The role of preoperative experience in neural function are discussed.Many brain lesion studies use animals that are naive with regard to the test challenge, and on the basis of the animal's response to the test, inferences are made about the role of particular brain structures in the behavior. A more "dynamic" approach was used by Benjamin (1959). In his study, groups of rats with cortical ablations were given various degrees of preoperative experience in a taste discrimination test. The results showed that the more preoperative experience with this test, the less likely there would be a taste discrimination deficit; rats that were not given this preoperative experience did show this deficit.Similarly, recent studies on diencephalic lesions indicate that if one exposes rats to an experimental test prior to induction of the lesion, the rats when tested postoperatively respond appropriately to the test whereas rats not given the preoperative experience do not (

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“…Despite increasing the concentration of quinine in the diet until deaths ensued in both control and lesioned groups, we were unable to drive the body weights of lesioned rats below those of controls. Adaptation to test solutions (Singh, 1974) or behavioral situations (King & Gaston, 1973;Singh, 1973) before lesioning, however, can alter postsurgical behavior . In Experiment 1, the exposure to lower concentration quinine diets (e.g., .4%, .6%) that occurred after surgery might have served to adapt the animals to the quinine-adulterated diets, so mitigating effects that might otherwise have been seen at the higher concentrations.…”

Section: Resultsmentioning

confidence: 99%