Twenty-one healthy women were studied during one menstrual cycle in order to determine whether cortisol and growth hormone responsivity to psychological stress was related to estrogen levels. Blood was drawn approximately three times per week for analysis of estradiol, progesterone, cortisol, and human growth hormone. During either the menstrual or intermenstrual phase, each subject participated in an interview that was designed to be mildly stressful. State and trait anxiety were assessed using the Spielberger State-Trait Anxiety Inventory. Anxiety state was measured prior to and immediately following exposure to the psychological stress; trait anxiety was assessed at the end of the study. Cortisol and growth hormone responses to the psychological stress were not related to menstrual cycle phase. Anxiety levels were also independent of menstrual cycle phase. Subjects who displayed significant cortisol and/or growth hormone responsivity to the interview had significantly higher anxiety levels post stress than did nonresponders, although anxiety level prior to the interview was not different for the two groups.

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The hypothalamic regulation of feeding behavior is thought to involve a continually active lateral feeding center which induces a sustained manifest urge to eat and a relatively quiescent ventromedial satiety center which, when activated, suppresses this urge.' lo It has been suggested that the satiety signals originate as a result of the effect of glucose a t specific glucoreceptor sites in or on the cells of the ventromedial center.''-''In 1949, Brecher and WaxlerI6 observed that a single intraperitoneal or subcutaneous injection of goldthioglucose produced hyperphagia and obesity in mice. Marshall, Barrnett and Mayer" confirmed this observation and found that the animals with goldthioglucose-induced obesity had central nervous system damage involving the ventromedial nucleus of the hypothalamus, the ventral part of the lateral hypothalamic area, the supraoptic nucleus, the arcuate nucleus, and the median eminence. Since neither ventromedial lesions nor hyperphagia nor obesity was produced by goldthiogalactose, goldthiosorbitol, goldthiomalate, goldthioglycerol, goldthiocaproate, goldthioglycoanilide or goldthiosulfate, Mayer and Marshall" suggested that the ventromedial neurons of the hypothalamus manifest a specific affinity for the glucose component of the molecule, and that these glucose receptive cells were destroyed by the toxic gold moiety of the molecule.In 1961,'47'' utilizing the techniques of neutron radioactivation and radioautography, we found that in animals which had been previously treated with goldthioglucose and had become hyperphagic and obese, gold was deposited in the ventromedial area of the hypothalamus. None of the animals treated with goldthiomalate became hyperphagic and obese, none exhibited hypothalamic localization of gold, but all manifested diffuse gold distribution throughout the brain. These experiments showed that, although both goldthioglucose and goldthiomalate are diffusely distributed throughout brain tissue, only goldthioglucose is specifically accumulated in discrete areas, one of which is the ventromedial area of the hypothalamus.In the present work we employed a neutron activation technique and radioautography correlated with metabolic studies to determine quantita-*Research supported by the U. S. Atomic Energy Commission ?Advanced research fellow of the American Heart Association 485