In the mouse, perinatally present testicular androgens promote the development of the propensity for adult intermale aggression. In the newborn male mouse plasma testosterone more than doubles during the first 2 h after birth and then falls rapidly to remain relatively low for the remainder of the 24-h period after birth. To study whether this surge in plasma testosterone influences aggressiveness we castrated some male mice within 1 h after birth i.e., before the surge. We castrated other males between 1.5-6 h after birth, or 1, 6, or 12 days after birth. Males were given testosterone as adults and tested for aggression for 5 weeks. Males castrated within 1 h after birth were not clearly different from males castrated 1.5-6 h after birth with respect to aggressive behavior, although males in both groups were substantially less aggressive than males castrated later in life. Thus, the perinatal surge in plasma testosterone in the mouse does not appear to make a unique contribution to the organization of mechanisms for intermale aggression. Rather, this surge is probably the initial stimulus that begins the postnatal process by which testicular hormones promote the development of the potential for adult aggressive behavior. This process appears to be complete by 6 days after birth.

In the rat an abrupt discharge of testicular testosterone in the newborn male figures prominently in the development of mechanisms controlling gonadotropin secretion, sexual behavior, and also promotes the functional differentiation of the accessory sex glands. In this study we detail the temporal characteristics of this surge in the rat, and we provide comparative data documenting a similar surge-like appearance of testosterone in neonatal male mice, recently foaled male horses, and newborn human infants.Although the physiological and behavioral significance of this phenomenon for species other than the rat remains to be determined, the apparently ubiquitous appearance of the neonatal testosterone surge suggests that it may be of special significance in the sexual differentiation of many mammalian species.

Blood was obtained by heart puncture from 19-day-old Black Sex link chicken embryos and from Black Sex link chickens at 1.5, 6, or 24 h post-hatching. Plasma testosterone was determined by gas chromatography-mass spectrometry associated with stable isotope dilution. At 19 days the plasma of male and female chick embryos contains measurable amounts of testosterone and levels do not differ between sexes. After hatching plasma testosterone gradually declines from pre-hatch concentrations in males and females, but in all the post-hatch ages studied, plasma testosterone was significantly higher in male than in female chicks. These results indicate that in male chickens, contrary to mammals at birth, there is no surge in plasma testosterone at hatching.

The variations of the testicular responsiveness to hCG and the implication of the maternal estrogens in the functioning of the testes were studied in the perinatal male rat. Male rat fetuses treated with hCG at the end of gestation failed to show an increase in serum testosterone (T). The lack of testicular responsiveness to hCG in the fetus is neither due to anesthesia nor to a blocking effect of estrogens directly on the testes. On the other hand, hCG injected either at 4 h or at 48 h after birth increases serum T. The administration of 5 mug of estradiol 17beta (E2) to the newborn male rat at the time of birth blocks the expression of the postpartum testosterone surge. The fall in the plasma estrogens and the increase of the testicular sensitivity to gonadotropic stimulation at the time of birth are factors which are very likely implicated in the determinism of the neonatal testicular hyperactivity.

Blood was obtained from human male and female neonates within a few minutes after birth, and at intervals thereafter for up to 21 h. Serum LH was substantially higher at birth for boys than girls. For most boys, serum LH fell precipitously during the next hour; serum LH remained low for the remainder of the period sampled in both boys and girls. In girls, serum testosterone was low at birth and remained low for at least 21 h. At birth, serum testosterone in boys was higher than for girls, increased dramatically during the first 3 h after birth, and remained elevated (2 to 3 times higher than for girls) between 3 and 12 h after birth. In newborn human males, a sudden discharge of hypophyseal LH appears to stimulate neonatal secretion of testosterone by the testes. The functional significance of this phenomenon remains to be determined.

Newborn female and male C57BL6 mice were decapitated at birth or at different times during the first 24 h after birth and testosterone was determined by radioimmunoassay in plasma and testes. In newborn females, plasma testosterone is low and does not significantly change over the first 24 h after birth. In contrast, in newborn males, plasma testosterone more than doubles during the first 2 h after birth and then falls rapidly to remain relatively low for the remainder of the 24 h period after birth. The increase in plasma testosterone is of almost certain testicular origin since it follows a decrease in testicular testosterone content. It seems likely that the increase in plasma testosterone in male mice which reaches its peak at 2 h after birth is involved in an essential way in the development of well-documented sex differences in gonadotropin secretion and behavior.

Pregnant female rats were injected with progesterone or oil from 18.5 up to 21.5 days of gestation. Rat pups were delivered by caesarean section, and pups delivered from progesterone-treated mothers were injected with 100 micrograms of progesterone and pups from oil-treated mothers were injected with oil. Two hours after delivery, pups were killed and hypothalamic testosterone and estradiol were determined by RIA. Control males had substantially higher concentrations of testosterone and estradiol in hypothalamus than control females. Treatment with progesterone did not affect the accumulation of testosterone in the hypothalamic tissue of neonatal males, but completely prevented the formation of estradiol in hypothalamic tissue. This result suggests that progesterone can inhibit hypothalamic aromatase activity in the neonate and may explain why progesterone can protect against some of the neural defeminizing effects of neonatally administered androgens.

In the male rat, a dramatic increase in serum testosterone of testicular origin occurs during the first two hours of postnatal life. This experiment was designed to determine whether this increase contributes to the development of the propensity for adult male rats to mount sexually receptive females. Male rats were castrated at either 0-hours (virtually at the moment of birth), or at 6 hours, or at 24 hours after birth. Some males castrated at 0-hours were injected with 1 microgram of testosterone after surgery. Control males were sham-operated at birth, and castrated in adulthood. At about 90 days of age, each male was given testosterone replacement therapy and tested over a period of 6 weeks for mounting. Castration of newborn males retards the development of mounting in the sense that males castrated at 0-hours require a longer period of hormone stimulation before beginning to mount, a greater percentage of males castrated at 0-hours fail to mount altogether, and even those who do mount do so at a frequency significantly lower than that for males castrated later in life. These effects are not seen when males are given an injection of testosterone immediately after castration at 0-hours, or when castration occurs at 6 hours after birth or later. We conclude that gonadal hormonal stimulation during the first several hours after birth contributes to, although is perhaps not essential for, the development of mounting.

In the neonatal male rat, a rapid and transient increase in serum testosterone occurs about 2 h after birth. This post-partum testosterone surge (PPTS) has been implicated in the masculinization and defeminization of the central nervous system. The present study shows that environmental temperature can have a profound influence on the PPTS. Male rats were delivered from their mothers by caesarean section on day 22 of gestation. Immediately thereafter, neonatal males were placed at an ambient temperature of either 18, 21, 24 or 30 degrees C. With 2 h of exposure, the body temperature was in close correspondence with the ambient temperature. The PPTS was clearly abolished in the pups exposed for 2 h at either 18 or 21 degrees C. The effect of temperature was reversible: by placing pups at either 18 or 21 degrees C for 2 h after delivery, and then rewarming by placing them with a foster mother, the PPTS was delayed until 4 h after birth, i.e. 2 h after the beginning of rewarming. Thus, environmental cooling appears to retard the development of neural and/or endocrine systems mediating the PPTS. Aberrant maternal care which would produce substantial cooling of the male pups would be expected to affect the PPTS, which in turn might affect the sexuality of male progeny.

Thirty children acutely infected by Plasmodium falciparum and suffering either benign uncomplicated malaria (17 cases), or cerebral malaria (13 cases), were investigated for T-cell number and subset distribution among peripheral blood mononuclear cells using OKT3, OKT4, and OKT8 monoclonal antibodies, and for natural killer (NK) activity using K562 cells as targets. They were compared to a group of 16 age- and sex-matched healthy Senegalese children. OKT8 cell percentage was found increased in both groups of patients with a decrease of OKT4 cell percentage in cerebral malaria patients only. Both groups thus exhibited a decreased OKT4OKT8 ratio, which was slightly lower in cerebral malaria cases than in benign cases. NK activity was found elevated in uncomplicated cases of malaria, in contrast to patients suffering cerebral malaria, who exhibited a profound depression of NK activity.

Neonatal male rats were castrated either at 0, 6 or 24 hrs. after birth. As adults, testosterone was delivered by subcutaneous implantation of a Silastic capsule containing this hormone. The probability to display mounting behavior in presence of an estrous female was lower when the animals were castrated at 0 hr. than at 6 or 24 hrs. or when they received a subcutaneous injection of 1 microgram of testosterone propionate, at the time of castration at 0 hr. These results suggest that in the rat, during the 6 hrs. following birth, neonatal testes influence the sensitivity of the adult central nervous system to testosterone.

In the hibernating ground squirrel activity of adrenal dopamine-beta-hydroxylase was significantly lower as compared with the active animals (P less than 0.01). The highest activity of this enzyme was found in animals tested immediately after arousal from hibernation (P less than 0.01). The adrenal weight was higher in hibernating animals than in the active or aroused ones. The difference between the active and aroused animals was significant (P less than 0.01). Extremely high enzyme activity was found in the adrenals of animals exposed to continuous light for 3 weeks as compared with active animals kept in continuous darkness or with controls subjected to a regime of 12 hr light - 12 hr darkness (P less than 0.01). The weight of the adrenals in the three groups was about the same level.

Endogenous concentrations of testosterone (T), 5 alpha-dihydrotestosterone, progesterone (P), and estradiol-17 beta (E2) were determined with specific RIAs in serum and hypothalami of male and female rats before, during, and up to 24 h after birth. In the male, a dramatic and transient increase in T concentration was observed in the serum and the hypothalamus between 0 h in utero and 2 h after delivery. At all times studied, T levels were undetectable in the female. We failed to detect any significant 5 alpha-dihydrotestosterone levels in the serum and the hypothalamus of both sexes. Serum E2 levels decreased between the 21-day fetal stage and 24 h postpartum. However, in males, hypothalamic E2 dramatically increased between 0 h in utero and 1 h after delivery and decreased between 2 and 24 h. This surge was absent in females and males gonadectomized at 0 h, suggesting that this surge is linked to the presence of the testes. E2 was undetectable in the cerebral cortex. P presented the same pattern of declining levels in the male and the female, and no sex difference was noted for the mean concentrations in the serum or the hypothalamus. The fall in P levels and the sudden increase in hypothalamic T and E2 levels could be determinant factors in the initiation of central nervous system sexual differentiation in the rat. The fact that in the male rat, hypothalamic E2 increases during the time when testicular secretions defeminize the brain strengthens the view that E2 mediates some of the effects of T.