Testicular atrophy (TA) and decreased plasma luteinizing hormone (LH) levels were observed in the adult male rat after treatment with 500 µg of estradiol benzoate (EB) on the first day of life, while administration of 1 mg of testosterone propionate (TP) on the same day was also associated with TA but increased LH levels. TA and no changes in plasma LH levels were seen when the treatment was performed with similar doses of both steroids on day 5 of life. In no case were plasma follicle-stimulating hormone (FSH) levels altered by these treatments. No differences in basal LH and FSH levels were found in adult females after treatment with 100 µg of EB or 1 mg of TP on day 5. LH response to castration was lower in neonatally androgenized and estrogenized adult male and female rats than in their respective controls, while FSH response was scarcely modified. In conclusion, neonatal treatment with EB or TP in both sexes induced alterations in LH control mechanisms without changing those of FSH.

enzyme cleaving the side-chain of cholesterol (rate limiting step in steroidogenesis) was considerably reduced in the diabetic state (59%, p < 0.002) and insulin treatment restored it to even supranormal levels (not significant). Our findings suggest that insulin may play a physiological and differential role in regulating the secretory activity of the anterior pituitary. The insulin is needed for normal LH and prolactin release and Leydig cells function but its role in FSH release and Sertoli cells function is not clear.

Neonatally oestrogenized female rats showed hyperprolactinaemia (prolactin, 230 micrograms/l), normal LH levels and absence of a positive feedback effect of oestrogen on secretion of LH at 5 months of age. Bromocriptine treatment for 13 days (1 mg/kg per day) caused no changes in LH levels and prolactin levels decreased to normal values (33 micrograms/l). This decrease in prolactin concentration was not followed by the recovery of phasic LH response to oestrogens. The effectiveness of oestrogens to induce prolactin secretion was greater in the neonatally oestrogenized rats than in the control group. In both cases the effect diminished after bromocriptine treatment. These results indicate that hyperprolactinaemia is not the cause of the anovulatory state in oestrogenized rats and that neonatal treatment with oestrogens alters oestrogen--prolactin relations, probably involving dopamine.

The role of the serotoninergic system in the control of LH, FSH and prolactin secretion was analyzed in control and neonatally estrogenized male rats. Animals injected s.c. with 500 µg of estradiol benzoate (EB) on day 1 of life, or their corresponding sham-treated controls, were divided on day 75 into the following groups: (1) orchidectomized; (2) injected intraventricularly with 5,7-dihydroxytryptamine (5,7-DHT); (3) orchidectomized and treated with 5,7-DHT, and (4) sham operated. 15 days later, the animals were decapitated and their FHS, LH and prolactin plasma values measured by specific RIA systems. After the treatment with 5,7-DHT, control animals showed a decline in basal prolactin levels but no modification in basal LH and FSH values. After castration, 5,7-DHT-treated animals showed a reduced LH increase and a more marked prolactin decrease. In neonatal estrogen-treated animals, the 5,7-DHT injection did not change FSH, LH or prolactin levels but did partially or completely abolish the post-castration rise in FSH and LH levels, respectively. These data seem to indicate that neonatal estrogenization induced a modification of the serotoninergic role in the control of LH, FSH and prolactin.

Neonatal estrogenization induced in prepubertal males atrophy of the testis and ventral prostate and increased the weight of the seminal vesicles. Atrophy of the testis was probably due to the inhibition of FSH and LH secretion: males estrogenized on day one and sacrificed daily from day six to day fifteen showed lower gonadotropin levels than their respective controls. In addition, daily FSH and LH administration (80 ,ug/lOO g BW and 40 pg/IOO g BW respectively) from day one to day fifteen increased testicular development more effectively in estrogenized than in control males and the differences between the two groups disappeared. Prostate atrophy was due to the decreased testosterone secretion. The reason for the hypertrophy of the seminal vesicles remains unclear: reduction in Prolactin levels due to bromocriptine treatment did not normalize the seminal vesicles weight, indicating that hyperprolactinemia was not the cause. Male rats estrogenized on day one, orchidectomized on day 5 and decapitated on day fifteen also showed hypertrophy in their seminal vesicles. These results indicate that testicular factors, other than testosterone, were not responsible for the vesicular hypertrophy. It seem possible that estrogens might act directly on vesicular growth. Mechanismen in der Bildung von prapuberalen Fortpflanzungsdefekten bei neonatal otrogenisierten mannlichen RattenZusammenfassung: Die neonatale Ostrogenisierung ruft bei prapuberalen mannlichen Ratten eine Hodenatrophie und eine Atrophie der ventralen Prostata hervor bei gleichzeitigem Gewichtsanstieg der Samenblasen. Die Hodenatrophie wurde wahrscheinlich durch eine Hemmung von FSH und LH vemrsacht: Die ostrogenisierten Mannchen zeigten am ersten Tage sowie vom 6. bis 15. Tag herabgesetzte Gonadotropinwerte gegeniiber den Kontrollen. Dariiber hinaus ergab sich, daiS die tagliche Gabe von FSH und LH (FSH: 80 pg/lOO g kg und LH: 40 ,ug/ 100 g kg) vom ersten Tag bis zum 15. Tag zu einem Anstieg der Hodenentwicklung fuhrte, und zwar starker bei den ostrogenisierten Tieren. Die Prostata-Atrophie war durch die verminderte Testosteronsekretion verursacht. Die Ursache fur die Hypertrophie der Samenblasen bleibt unklar: so vermochte eine Reduzierung der Prolaktinwerte durch Bromokryptin keine Normalisierung des Samenblasengewichts herbeizufuhren; hieraus wird der SchluB gezogen, daB die Hyperprolaktinamie nicht etwa die Ursache sein kann. Mannliche Ratten, die ostrogenisiert wurden (am ersten Tag), die weiterhin am 5. Tag orchidektomiert und am 25. Tag dekapitiert wurden, zeigten gleichfalls eine Hypertrophie ihrer Samenblasen. Die Ergebnisse zeigen nach Auffassung der Autoren, daB die vom Hoden ausgehenden Faktoren, anders als Testosteron, nicht verant-Key words: Estrogenization, ratneonatal rat, estrogenization andrologia 19 (1987) Neonatal Estrogenization 23 wortlich sind fur die Samenblasenhyertrophie. Es scheint moglich, daB die Ostrogene direkt auf das Samenblasenwachstum wirken.