Atropine fails to block the overconsumption of sugar solutions by hypothalamic hyperphagic rats.

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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 3 out of 5 experiments, and in all experiments it suppressed their 24-h chow intake. The VMH rats continued to drink more of the sugar solutions than did the controls after all atropine treatments, and in 3 out of 4 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.