Abstract
Adult female rats given bilateral parasagittal knife cuts in the medial hypothalamus (VMH group) were hyperphagic and became obese on a chow diet, compared with sham-operated controls. The VMH rats also overconsumed, relative to controls, sucrose and glucose solutions during 30 min/day tests. Pretreating the VMH and control rats with atropine methyl nitrate (1.0, 5.0, or 10.0 mg/kg) reduced their intake of the sugar solutions in three out of five experiments, and in all experiments it suppressed their 24-hr chow intake. However, the VMH rats continued to drink more of the sugar solutions than did the controls after all atropine treatments, and in three out of four experiments their hyperphagia on the chow diet was not blocked by the atropine. The results do not support the hypothesis that vagally stimulated insulin release or other cholinergically mediated cephalic responses of digestion are essential for the expression of hypothalamic hyperphagia and finickiness.
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