282 /. /. Christian 



The growth form of these populations was approxunately sigmoid, indi- 

 cating that an intrinsic damping factor was operating to regulate and limit 

 the growth of populations throughout their histories. These populations 

 were started by introducing a small number of animals of both sexes into 

 confined quarters and allowing the population to grow of its own accord. 

 The populations were either sacrificed, at maxunal and submaximal levels, 

 to obtain organ weights and histologic material, or blood samples were 

 taken for eosinophil counts to assess functional changes, especially of the 

 adrenal cortex. 



The zonae fasciculatae of the adrenal cortices were hyperplastic and 

 hypertrophic in house mice of both sexes from populations of maximum 

 (asymptotic) size. The number and size of the cells of the fasciculata were 

 increased. Adrenal weight reflected the fascicular hypertrophy by increases 

 of 25% in the males and 14% in the females. The adrenal cortical hyper- 

 trophy was approximately half as great in mice from populations of approxi- 

 mately one half the maximiun size. 



The presence in mice of an adrenocortical X-zone which is involuted by 

 androgens has been described. This zone complicates the interpretation of 

 adrenal weight from immature or puberal male or nulliparous female house 

 mice unless histologic studies accompany the data on weights. In the case 

 of the freely growing populations of house mice there was a pronounced 

 hump in the adrenal weights in relation to body weights for mice from the 

 experimental populations in the 13-19.0-gm. weight range, even though the 

 fascicular hypertrophy was proportionately constant for all weights. The 

 curve of adrenal weight on body weight for the segregated control mice was 

 more or less regular with no pronounced irregularities, although there is a 

 tendency for the slope to decrease with increasing body size. This appar- 

 ently excessive adrenal hypertrophy in 13-19-gm. mice from intermediate 

 and high populations resulted from a failure of the X-zone to involute 

 normally rather than from a true hyperplasia or hypertrophy. The width of 

 the X-zone in segregated male house mice begins to decline in mice in the 

 10-12.9-gm. weight group, and involution is essentially complete by the 

 time a body weight of 16 gm. is reached. The decline did not begin in the 

 experimental animals until a weight of 16 gm. or more had been reached 

 and was not complete until a weight of 19 gm. Therefore, along with a 

 marked hyperplasia of the zona fasciculata, suggesting an increased secre- 

 tion of corticoids with increased density, there was a delay in the onset of 

 puberty, presumably with an insufficient production of androgens to in- 

 volute the X-zone of male mice. A great variety of steroid hormones, in- 

 cluding corticoids, have been tested for their ability to involute the X-zone 

 in male house mice (McPhail and Read, 19-42b; Antopol, 1953; Allen, 1954; 

 Christian, 1954) , but only those with pronounced androgenic activity (e.g., 



