Martha A. Mann

Infanticide: Genetic, developmental and hormonal influences in mice

Abstract DBA/2J and androgen-deficient C57BL/6J mice were examined for their response to newborn (1–3 day old) Rockland Swiss (R-S) albino mouse pups. Significantly more 70–90 day old C57BL male mice killed young as compared to similarly aged DBA males (80% vs 30% respectively). Adult, 70–90 day old, female mice of both strains typically retrieved newborn young to the nest site. Adult castration significantly reduced infanticide in males of both strains while exposure to testosterone (T)-containing silastic capsules restored it. Treatment of adult ovariectomized female mice of both strains with T-containing capsules significantly elevated the exhibition of pup killing. When tested for infanticide at 25, 35, 45, 55 or 65 days of age, few males of either strain killed young at 25 days of age. However, beginning at 35 days of age, significantly more C57BL males killed young at every age as compared to DBA males. Moreover, C57BL males exhibited an earlier developmental onset of adult-like levels of infanticide than DBA males (45 vs 65 days of age respectively). Finally, older (4.5 to 7 months of age) DBA males exhibited levels of pup-killing identical to that of younger (2 months of age) C57BL males (70%). The findings are discussed in terms of their relationship to other sexually dimophic T-dependent masculine behaviors. The potential importance of infanticide for rodent reproductive strategies and population regulation is also considered.

Infanticide: Accounting for genetic variation in mice

Infanticide, the killing of young, is one of a number of sexually-dimorphic traits in mice that is dependent upon androgen stimulation during perinatal life and during adulthood. Genotype also influences infanticide in that males of some strains of mice (C57BL/6J) exhibit high levels of this behavior while males of other strains (DBA/2J) seldom kill young. The experiments conducted here show that strain differences in pup killing behavior exhibited by males are not related to postweaning social factors nor are they due to differences in perinatal, pubertal, or adult levels of circulating hormones. These results, in combination with those previously reported, suggest that strain differences in the tendency of mice to kill young may instead depend upon the interaction of genotypic features such as prenatal hormone titers and/or sensitivity to these hormones, as well as on extra organismic factors such as intrauterine position. A model for understanding the manner in which genes and hormones may interact to influence infanticide and other hormone dependent sexually-dimorphic behaviors in mice is presented.

The role of progesterone in pregnancy-induced aggression in mice ☆

A series of six experiments was performed in order to explore the potential involvement of progesterone (P) in pregnancy-induced aggression (PIA) displayed by Rockland-Swiss mice toward adult male intruders. In Experiment 1, circulating levels of P and aggression were low on gestation Days 6 and 10 while both the behavior and the steroid reached peak levels by gestation Day 14. By gestation Day 18 (the day prior to parturition), serum P was at its lowest level yet aggressive behavior was still intense. Also, individual differences in the display of fighting behavior by pregnant females were not related to circulating P. Experiments 2 and 3 showed that supplemental P treatment to early pregnant female mice did not advance the onset of aggression. Experiment 4 showed that P treatment promoted the onset and elevated the incidence of aggression in virgin mice, but only in those females with intact ovaries. Experiment 5 showed that the aggressive behavior of P-stimulated virgin females was qualitatively and quantitatively different from that exhibited by pregnant mice in that the former exhibited fewer attacks and lunges than the latter. Finally, Experiment 6 showed that the removal of P from aggressive, P-stimulated virgins dramatically attenuated levels of the behavior. This contrasts sharply with the continued fighting behavior observed in late pregnant P-deficient mice. Thus, although P augments aggression in female mice it apparently is not a sufficient stimulus for producing pregnancy-like aggressive behavior.

Hormonal Influences on Maternal Aggression

With the exception of work conducted with female hamsters (see Floody, this volume), the study of the relationship between hormones and female aggressive behavior has never been of paramount importance. Recently, however, a number of investigators have turned to an analysis of this little-studied dimension of agonistic behavior. The results of this research tentatively suggest that female aggression during the peripartum period, like intermale aggression, is influenced by neuroendocrine status. The purpose of the present chapter is to review the available literature concerning the role of hormones in the aggressive behavior displayed by pregnant and lactating mammals. This review is limited to work conducted with hamsters, mice, and rats.

Prenatal testosterone exposure elevates maternal aggression in mice

Pregnant Rockland-Swiss (R-S) female mice were injected with oil, 0.5, 1.0 or 2.0 micrograms of testosterone propionate (TP) on days 12, 14 and 16 of gestation and the maternal aggressive behavior of their resulting female offspring was examined in adulthood. Prenatal exposure to 1 or 2 micrograms of TP, but not 0.5 micrograms of the steroid, significantly increased the number of attacks displayed by parturient mice toward adult male intruders. The behavioral effects on aggression were observed in the absence of effects on external morphology, body weight, or lactational performance. The findings support previous research showing that the development of feminine behavior may be sensitive to prenatal androgens. The possibility that the presence of fetal testosterone augments both male and female aggressive behavior is discussed.

A role for elevated plasma corticosterone in modulation of host response during infection with Trichinella pseudospiralis

Summary Suppression of host inflammatory response in mice infected with Trichinella pseudospiralis was associated with host plasma corticosterone levels significantly higher than those seen in uninfecled mice or in mice infected with T. spiralis. Increases in the population of mitochondria and depletion of lipid droplets in cells of the zona fasciculata were seen in the adrenals of mice infected with T. pseudospiralis. Elevations in enteritis, myositis and myocarditis accompanied 100% mortality in adrenalectomized mice infected with T. pseudospiralis, while lower levels of inflammation and no mortality were observed in sham operated or intact animals infected with this parasite. The severe myositis normally accompanying infection with T. spiralis was suppressed by concurrent infection with 1000 or 2000 T. pseudospiralis to levels equivalent to those seen in animals receiving 015 and 0‐41 mg cortisone acetate/25 g mouse/day, respectively.

Infanticide exhibited by female mice: Genetic, developmental and hormonal influences

Approximately 25-40% of 25-45 day old C57BL/6J females killed young (1-3 day old Rockland-Swiss (R-S) albino mouse pups) while similarly aged DBA/2J females were parental or ignored neonates. Beyond 45 days of age C57BL and DBA females seldom killed young. When ovariectomized at weaning and tested for infanticide at 65 days of age, DBA females rarely killed neonates while 40% of C57BL females exhibited the behavior. In contrast to DBA females, significantly more C57BL females killed young in response to the adult administration of testosterone propionate (TP) and estradiol benzoate (EB), but not dihydrotestosterone propionate (DHTP). It is tentatively proposed that strain differences in spontaneous and steroid aroused infanticide in female mice may be related to differences in the prenatal hormone environment.

Mice: suckling stimulation but not lactation important for maternal aggression

Two experiments were conducted in order to examine the role of nipple growth, suckling stimulation by young, and lactation in the maternal aggressive behavior displayed by Rockland-Swiss (R-S) Albino mice. Experiment 1 examined the aggressive behavior of parturient animals and separate groups of pregnant animals hysterectomized at various stages of gestation (Days 9, 11, 13, or 15) and fostered young. Aggressive behavior was present in pregnant animals hysterectomized and fostered young at a time when nipple growth was adequate for suckling to take place (i.e., after Gestation Day 11). In contrast, aggression was not evident in animals hysterectomized and fostered young at a time during gestation when nipple growth was inadequate for suckling to take place (i.e., on or before Gestation Day 11). Experiment 2 examined the aggressive behavior of separate groups of parturient animals fostered young for the first time 0, 1, 2, or 3 weeks postpartum. Parturient animals fostered young for the first time 1 to 3 weeks following parturition did not lactate but received suckling stimulation and exhibited aggression identical to that of animals fostered young for the first time immediately following parturition. The growth of nipples and suckling stimulation are necessary conditions for the display of meternal aggression in mice, but suckling-induced changes in lactogenic hormones may not be necessary.

Pup-killing behavior in mice: Suppression by early androgen exposure

Abstract Significantly more male mice castrated at birth killed newborn pups in response to adult testosterone propionate (TP) treatment than sham-operated controls. Female mice administered TP or estradiol benzoate (EB), but not testosterone (T), dihydrotestosterone (DHT), or dihydrotestosterone propionate (DHTP), on the day of birth killed significantly fewer young in response to adult TP than oil-treated controls. Neonatal MER-25 treatment prevented the suppressive effects of early TP exposure on T aroused pup-killing behavior. These data show that early androgen exposure attenuates the pup-killing producing properties of adult T and that aromatization of T to estrogen (E) during early life may mediate these effects.

Ergot drugs suppress plasma prolactin and lactation but not aggression in parturient mice

Abstract The daily administration of pituitary prolactin (PRL) inhibitors (ergocornine hydrogen maleate and 2-bromo-α-ergocryptine) to parturient Rockland-Swiss Albino mice suppressed circulating levels of PRL and lactation but failed to alter maternal aggression toward adult male intruders. The results suggest that, contrary to popular speculation, PRL may not be necessary for postpartum aggression in the mouse.