Because electrical stimulation of the lateral hypothalamus (ESLH) can elicit both feeding and reward, most investigators have concluded that stimulation does not evoke the aversive cues associated with hunger. It has been hypothesized, instead, that ESLH primes ingestion by evoking pleasurable taste sensations. A direct taste of this hedonic hypothesis was undertaken in rats that showed stimulus-bound feeding. Contrary to the prediction, it was found that the taste reactions (gapes, tongue protrusions, etc.) during ESLH were more aversive than hedonic. It is suggested that the stimulation influences behavior by potentiating the salience, but not the hedonic value, of external stimuli. The advantages of this incentive salience hypothesis are that it circumvents the need to postulate a hedonic sensory experience during stimulation and that it can explain how evoked feeding may switch to other behaviors when conditions are altered.

The view that stimulation of discrete hypothalamic areas elicits specific drive states is challenged by recent evidence. Data are presented to support the view that there is much less anatomical specificity within the hypothalamus than is commonly assumed. Significant differences between natural states of hunger and thirst and those associated with the elicitation of eating and drinking are described. Additional information related to species differences, the role of prior experience, and an analysis of the environmental conditions essential to the elicitation of well-established response patterns suggests an alternative interpretation of hypothalamic function in the regulation of behavior.

a biopsychologist who spent over 40 years studying "how the brain and other biological factors such as hormones and drugs influence behavior" (p. 6). He is not a psychotherapist, and in principle he is not against the idea of viewing and treating mental disorders from within a biological framework. (He does believe, though, that there is a need for a psychosocial component also-more of that later.)Originally he had set out to write a history of the interplay between the accidental discoveries of psychotherapeutic drugs and the set of scientific, psychosocial, and economic factors that within only a few decades had led to the drastic, wide-spread changes from practices that reflected a more or less psychodynamic orientation to those arising from the conviction that chemical events in the brain are "not only the cause of mental disorders, but also the explanation of the normal variations in personality and behavior" (p. 1).As he gathered material for his project, however, Valenstein noticed a recurring general pattern of scientifically and medically unacceptable work apparently abetted by a constellation of shoddy motives. Consequently, he expanded his plan to include questions concerning evaluation and motivation, such as: Does the evidence support the received views concerning the biological causes of disorders? Does it support the new biochemical theories of mental illnesses and the drug treatment approaches that evolved in the context of these theories? Who benefits from

Taste preferences of mature male and female rats for caloric and noncaloric sweet solutions have been found to differ. Although females do not drink more water than males, they consume significantly greater quantities of a slightly sweet 3 percent glucose and a very sweet 0.25 percent saccharin solution. When given a choice, males switch their initial preference for a saccharin solution to a preference for a glucose solution after several days, while females maintain a preference for the saccharin solution. Females also prefer significantly higher concentrations of saccharin than males do.

Lesions in the medial preoptic area of ovariectomized female rats reduced the quantity of estrogen needed to induce sexual receptivity in these animals. In addition, the number of days over which receptive behavior could be elicited after a single initial estrogen injection and with subsequent daily progesterone treatment was significantly increased by lesions in the medial preoptic area. These findings support the view that estrogen acts to reduce an inhibitory action that is tonically exerted by the medial preoptic area on pathways mediating estrous behavior.