Electrodes were implanted in the lateral hypothalamic feeding system; animals were subjected to both feeding and motivational tests. All animals that demonstrated stimulus-bound feeding behavior also showed high self-stimulation rates. As it was impossible to produce the feeding response without simultaneously producing the rewarding effect of hypothalamic stimulation, it was concluded that the feeding system of the lateral hypothalamus is one among a larger group of places where stimulation causes primary rewarding effects. With electrodes in these same areas, food deprivation often caused a major increment in the self-stimulation rate.

Small doses of the opiate antagonist naloxone selectively abolished overeating in genetically obese mice (ob/ob) and rats (fa/fa). Elevated concentrations of the naturally occurring opiate beta-endorphin were found in the pituitaries of both obese species and in the blood plasma of the obese rats. Brain levels of beta-endorphin and Leu-enkephalin were unchanged. These data suggest that excess pituitary beta-endorphin may play a role in the development of the overeating and obesity syndrome.

Increasing the palatability of food has two opposite effects: it promotes overeating and provokes caloric output (energy expenditure). The increase in energy expenditure is too small to compensate for overeating and, as a result, obesity occurs. Repeated administration of zinc tannate of naloxone, a long-lasting opiate antagonist, completely abolishes this diet-induced obesity in rats. The drug accomplishes this not only by reducing overeating but also by increasing energy expenditure. This suggests that endogenous opioid peptides encourage obesity in two ways—by stimulating appetite for palatable foods and by reducing energy expenditures.

No abstract

After systemic administration of several serotonergic antagonists, female rats that had been ovariectomized, adrenalectomized, and estrogen-primed showed lordotic responding. Lordosis could also be elicited after direct placement of serotonergic receptor blockers into hypothalamic sites known to contain serotonergic terminals. None of the treatments activated the soliciting component of the estrous behavior pattern of the female rat. It is postulated that the hypothalamus contains serotonergic terminals which suppress lordotic responding.