Meal initiation controlled by learned cues: effects of peripheral cholinergic blockade and cholecystokinin.
Sated animals can be induced to initiate meals by exposing them to external stimuli which they have learned, via Pavlovian conditioning, to associate with food. This study examined physiological properties of this control of feeding. The initial hypothesis examined was that conditioned feeding depended on the elaboration of cholinergic cephalic phase responses (e.g., anticipatory insulin secretion). This idea was evaluated by comparing feeding responses to presentation of conditioned cues following an injection of either a peripheral cholinergic blocker, atropine methyl nitrate, or a control substance, physiological saline. Peripheral cholinergic blockade had no effect on the meal initiated by presentation of conditioned cues even though the dose of atropine methyl nitrate used was demonstrated to be sufficient to completely suppress cholinergic cephalic phase responses. These results indicate that cholinergic anticipatory digestive secretions do not contribute to feeding in this preparation. The effects of exogenously administered cholecystokinin on feeding controlled by learned cues were also studied. Cholecystokinin suppressed the size of the meal induced by presentation of conditioned stimuli but did not influence the latency, or initial rate of eating. The implications of these results to a conclusion that cholecystokinin is a satiety factor are discussed.
D000818:Animals; D001286:Atropine Derivatives / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology*; D003214:Conditioning, Classical; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000187:drug effects; D005744:Gastric Acid / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009407:Nerve Block; D010275:Parasympathetic Nervous System / Q000502:physiology*; D051381:Rats; D012527:Satiation
D001286:Atropine Derivatives; D007328:Insulin; C006649:methylatropine; D002766:Cholecystokinin