Discussions 



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existed that insufficient concentrations of gonadotropin were stored in the pituitary 

 to cause ovulation when released on hypothalamic stimulation. In order to assure 

 sufficient gonadotropin storage, six sterile rats were pretreated with progesterone in 

 a dosage calculated to block the secretion of gonadotropin (2 mg s.c. in oil). This 

 dosage of progesterone interrupted the persistent vaginal cornification and generally 

 induced 3 days of diestrus followed by a single day of proestrus. When no further 

 treatment was given, all rats returned to the persistent-estrous condition. If, however, 

 the median eminence was stimulated on the day of proestrus, ovulation occurred in 

 all animals (Fig. 3). Progesterone alone did not cause ovulation. It is apparent, there- 

 fore, that the sterile rat pituitary can function normally provided (a) proper gonado- 

 tropin storage is permitted and (b) an impetus for its release is supplied by the 

 hypothalamus. 



Once assured that the progesterone-primed sterile rat could be induced to ovulate 

 on hypothalamic activation, we made a more specific study of the hypothalamic 



Fig. 6. Midsagittal reconstruction of rat hypothalamus indicating extent of area which 



when stimulated resulted in ovulation. Abbreviations: Hippo, Hippocampus; M, Massa 



intermedia; PV, Paraventricular nucleus; SP, Septum; II, Optic nerve. 



regions which would cause ovulation when stimulated. In this preparation, the positive 

 areas were found to occupy an area just rostral and caudal to the ventral medial and 

 arcuate nuclei (Figs. 4, 5, 6). Stimulation of the medial or lateral preoptic areas or the 

 mammillary body regions did not induce ovulation nor did stimulation of the lateral 

 hypothalamic or median forebrain bundle regions. These results are contrasted to those 

 of Everett in which ovulation could readily be induced by stimulation of the preoptic 

 area. This discrepancy raises several questions : (a) It has been demonstrated that the 

 malfunction in the ovulatory mechanism of the androgen-sterilized rat is not resident 

 in the adenohypophysis as such, but more likely at the hypothalamic level. Does the 

 failure of the preoptic region of this animal to induce ovulation in response to stimu- 

 lation indicate the site of "masculinization" ? (b) What specific structures are being 

 stimulated in the preoptic area to cause adenohypophysial activation in the normal 

 rat? The amygdala is known to contribute efferent fibers via the stria terminalis to 

 the hypothalamus and it has also been implicated in the control of ovulation. Is it 

 this tract which is being stimulated, and if so can ovulation be induced by preoptic 

 stimulation in animals with amygdaloid lesions in which fiber tract degeneration 



