Androgen dependence of growth and epithelial morphogenesis in neonatal mouse bulbourethral glands.

The early development of the mouse bulbourethral gland (BUG) and the role of testosterone (T) in the normal growth and epithelial morphogenesis of this male accessory sex gland were examined. The mouse BUG differentiates from the urogenital sinus on day 17 of gestation (vaginal plug = day 0; birth = day 19), and initially consists of a solid epithelial rudiment encased in a large condensed capsular mesenchyme. The epithelium begins to branch and canalize on day 1 postnatally, and the branches enlarge and become more numerous on days 2 and 3. On day 4, secondary branches appear, and by day 6, the epithelium has become extensively arborized and almost fills the mesenchymal capsule. The BUG increases 3.9-fold in DNA content from day 0 (day of birth) to day 6 postnatally; the epithelium grows proportionately more than the mesenchyme during this period (12-fold vs. 2.3-fold). Growth of BUGs in mice castrated at birth or castrated and then treated with cyproterone acetate, an antiandrogen, over the first 6 days of life was reduced by 80%, but not abolished. Thus, the growth of the BUG is partially independent of androgens during early neonatal life. However, morphogenesis of the BUG epithelium is totally abolished in neonatally castrated mice. T replacement given to neonatally castrated mice during days 0-6 restored development to normal. T injections also reinitiated growth and morphogenesis in developmentally retarded BUGs from 6-day-old neonatally castrated mice. The partial dependence of the neonatal BUG on androgens for growth is similar to that seen in the prostate, which is also derived from the urogenital sinus. In contrast to the prostate, where neonatal castration reduces but does not abolish epithelial morphogenesis, androgen deprivation completely abolished epithelial morphogenesis in the neonatal BUG. (Endocrinology 121: 2153-2160, 1987).