The sexual maturation of male prairie deer mice (Peromyscus maniculatus bairdii) that were reared with other males was inhibited in comparison with that of males reared in isolation. Inhibition occurred in males reared with nine or four males of the same age, as well as in those housed with one adult male. This phenomenon was observed after several periods of grouping, and consequently at several ages ranging from 5 wk to 4 mo. Females did not retard the sexual development of males. These results indicate that the sexual maturation of individual deer mice is modulated by the specific composition, rather than density, of the local group. Cole (1954), in his analysis of the influence of life-history traits upon population dynamics, found the age at which animals first reproduce to be particularly important. In species having relatively short prereproductive periods, a modest change in the age at first reproduction markedly alters the reproductive potential of a population. This age is not a fixed characteristic of a species, as Cole assumed for the purpose of his illustrative calculations. A number of reports document a delay of sexual maturation in populations at peak density compared with those in which numbers are still increasing (Christian, 1971;Krebs & Myers, 1974). Density-dependent retardation of sexual maturation has been advocated as a major mechanism in the regulation of population growth (Christian, 1971). Laboratory investigations are required in order to determine the nature of this influence of density upon the sexual maturation of individual members of a population. The regulatory influence of conspecificsThis study was submitted by the first author to North Carolina State University in partial fulfillment of the requirements of the master's degree. We are indebted to P.

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Morphological and behavioral responses to estradiol-17/3 (Ez-ll/3) and estradiol-17a (E2-17«) were examined in a series of three experiments. The Ea-17/3 augmented uterine growth in hamsters to a greater extent than did E2-17a. Lordosis in ovariectomized adults was elicited by treatment with Eg-17/3 but not with E2-17« (each tested in combination with progesterone). When administered neonatally, only E2-17/3 disrupted estrous cyclicity in the intact female and induced the ability to mount in ovariectomized, androgen-treated adults. These results suggest the existence of a stereospecific response to estrogenic stimulation in neural tissue comparable with that occurring in the uterus.The specific molecular requirements of estrogen-sensitive sex ducts of female mammals have been investigated in some detail. Studies of rodent uteri have demonstrated the existence of a cellular receptor for estadiol-17/3 (E 2 -17/3) that interacts only weakly with nonestrogenic steroids. Although less effective than E 2 -17^, other estrogens compete with radiolabeled E2-17/8 to varying degrees for binding to the E2-17/3 receptor (Gorski, Toft, Shyamala, Smith, & Notides, 1968). The estrogen estradiol-17a (E2-17a) has been particularly useful in the study of estrogen binding in the uterus. Although differing from E2-17/3 only in the position of the hydroxyl group at carbon 17, Ea-17o! competes poorly for binding to the E 2 -17 (3 receptor (Noteboom & Gorski, 1965;Puca & Bresciani, 1968;Terenius, 1965), a result that indicates the high degree of stereospecificity of the estrogen-uterus interaction.The stereospecificity of estrogenic stimulation of neurobehavioral processes has