Evidence is presented for the depressant effect of amphetamine on food consumption and food-motivated behavior, as well as for the facilitating effect of the drug on intellectual and motor performance, personality and social behavior, bodily activity, peripheral systems, avoidance conditioning, and escape behavior. Since reversal or inconsistent effects are also noted with large dosages of amphetamine and with differences in experimental procedure, guidelines for future investigation are suggested in terms of (a) an increased attention to the relation of dosage and effect, and (b) the need for considering the specific experimental conditions under which the drug is employed.

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The hypothalamic regulation of feeding is discussed in terms of the ventromedial hypothalamic "satiety center" and the lateral hypothalamic "feeding center." Two hypotheses concerning the anorexic properties of amphetamine are considered in terms of the drug's interaction with hypothalamic centers-a ventromedial-hypothalamic-mimicking hypothesis and a lateral-hypothalamicblocking hypothesis. A consideration of these hypotheses suggests that the drug influences both centers, and that additional sites in the cerebral cortex and brainstem also may serve ancillary functions in mediating the drug's effect on feeding. It is suggested that future research should attempt to clarify the mediational processes underlying the drug's effect on feeding and nonfeeding performance and, in those instances where such processes overlap, to specify the nature of the overlap.The general depressant effect of amphetamine on feeding and food-motivated behavior is well established (Cole, 1967(Cole, , 1970. Carlton (1963) has suggested that amphetamine anorexia may be due to an increase in activation to the degree that responses incompatible with those required in feeding occur and thus result in a decrease in feeding. A second peripheral view of the action of amphetamine on feeding (Mogenson, 1968) suggests that the drug reduces liver and muscle glycogen and thereby increases the intracellular glucose in hepatic cells that causes gluco-receptors in the liver to signal a state of satiety. Such peripheral interpretations must be given proper consideration, but they do not explain the changing effectiveness of amphetamine on feeding following central nervous system lesions (Cole, 1967(Cole, , 1968. Furthermore, amphetamine has been observed to depress feeding in the complete absence of peripheral changes in the circulatory system (Nathanson, 1937) and after interruption of nerve pathways regulating the gastro-intestinal tract (Harris, Ivy, & Searle, 1947).1 Preparation of this paper was supported, in part, by a Faculty Fellowship from the Rutgers University Research Council.2 The author thanks Dr. John R. Brobeck for stimulating discussions on the topic and for his reading of the original manuscript.Reprint requests should be sent to Sherwood 0.

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