Ventromedial hypothalamic lesions eliminate gastric acid secretion elicited by anticipated eating
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Electrolytic lesions of the ventromedial hypothalamus (VMH) produce an obesity syndrome characterized, in part, by excessive food intake and adiposity. Several hypotheses suggest that VMH lesion-induced hyperphagia results from elevated parasympathetic tone on the viscera expressed via the vagus nerves. To evaluate this possibility, vagally-mediated gastric acid secretion was measured in control and VMH-lesion rats. Initially, Pavlovian conditioning was used to elicit acid secretion to anticipated eating. VMH lesions eliminated the ability to mobilize acid secretion to the expectation of eating even though other behavioural indices of conditioning indicated that VMH rats still expected the food. The generality of the acid secretory deficit in VMH rats was evaluated by activating vagally-mediated acid secretion pharmacologically with insulin or 2-deoxy-D-glucose (2DG). VMH rats significantly increased acid secretion to insulin, although the response was attenuated compared to controls. Acid secretion stimulated by 2DG was normal. Thus the effects of VMH lesions on vagally-mediated acid secretion depend on the way in which the response is activated. The implications of this finding are discussed.
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