292 J. J. Christian 



groups. In these experiments the weights of the preputial glands of mice 

 from populations of high density were significantly greater than those from 

 segregated controls. For their stimulation to full development and function, 

 the preputial glands depend primarily on the more potent androgens (Bur- 

 rows, 1949), but the weakly androgenic steroids (Huggins et al., 1955), 

 ACTH (Jacot and Selye, 1951; Asling et al., 1951), and pituitary growth 

 hormone (Huggins et al., 1955) all have a mild stimulatory action on the 

 preputials. The evidence for the effects of estrogens on the preputials is 

 conflicting. On the one hand, estrogens appear to have a mild stimulatory 

 action (Burrows, 1949; Beyler and Szego, 1954) whereas other experiments 

 indicate that they inhibit the preputials (Rennels et al., 1953). Since other 

 evidence from the experiments with mouse populations indicates that the 

 production of sex steroids by the gonads and growth hormone by the pitui- 

 tary is inhibited at high densities, it seems probable that the increased size 

 of the preputials in these intact females must have been due to increased 

 ACTH and possibly increased adrenal C19 steroids. In any event the data 

 on the preputials are strongly suggestive of increased pituitary-adrenocorti- 

 cal function. Attention should be directed to the fact that the preputials 

 were appreciably larger than those from segregated mice with full reproduc- 

 tive competence. Therefore there is no reason whatsoever to implicate estro- 

 gens in these effects ; so ACTH and adrenal androgens must be responsible 

 for stimulating preputial development to well above the control levels. 

 Presumably the levels of estrogens declined in these females as a result of 

 a decreased secretion of pituitary gonadotropins in association with in- 

 creased secretion of ACTH. These conclusions were supported by the fact 

 that there was also (1) a marked increase in the proportion of females of 

 adult size with infantile uteri and ovaries, and (2) a 20% decline m 

 number of females with mature reproductive organs that were also preg- 

 nant, (3) a 13% decrease in the mean number of viable embryos per 

 pregnancy, and (4) a 58% increase in the number of resorbing embryos per 

 pregnancy. Thus there was diminished fertility and increased losses between 

 o\'ulation and implantation, and implantation and birth. Decreased fertility 

 was shown in some animals by a total inhibition of reproduction and in 

 others by a markedly diminished number of viable embryos per pregnancy. 

 These results agree with those of Crowcroft and Rowe (1957). The same 

 phenomena apparently occurred in populations of voles (Clarke, 1955; 

 Louch, 1956; Christian, 1959b) . Birth rates declined steadily as the popula- 

 tions increased for house mice and voles (Christian, 1959b, 1961). There- 

 fore it seems that reproductive function is inhibited in female mice and voles 

 in proportion to population density, either in terms of the proportion of 

 reproductively competent adult females in a population or of the degree of 

 reprodu(•ti^'e function in individuals. Stated another way, reproductive 



