Open-field behaviour in chickens: A replication revisited

In an attempt to show that the open field can still be used as a valid measure of fear, Jones (1983) has reported a failure to replicate some of our findings. The present studies show that this was due to procedural and methodological differences. For instance, we found that birds tested in a novel environment behaved quite differently from those, as in Jones' case, which were placed in one resembling the home cage. Moreover, birds housed in isolation for two days prior to testing reacted differently than those, as again in Jones' case, which were reared in isolation from hatching to the time of testing. The results were interpreted as being consistent with our view that open-field behaviour reflects a conflict between the need to reinstate contact with conspecifics on the one hand, and evade predation on the other.     

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.     

Steroidal influences on pup-killing behavior in mice

Four experiments were conducted in order to examine the biochemical pathway through which testosterone (T) acts to produce pup-killing behavior in ovariectomized female mice. Estradiol benzoate (EB) and testosterone propionate (TP) were both effective in stimulating the pup-killing response (Experiment 1). The nonaromatizable androgen dihydrotestosterone (DHT) and the aromatizable androgen testosterone (T) were equipotent in eliciting the behavior while the nonaromatizable androgen androstanedione (AA) was ineffective (Experiment 2). Pup-killing behavior was activated by the aromatizable androgen androstenedione (AE) but only if it was administered chronically at very high doses (Experiment 3). The combination of subthreshold doses of EB and DHT synergized to produce the pup-killing response (Experiment 4). These findings suggest that both aromatization and reduction may be important for the stimulation of pup-killing behavior in mice.     

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

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.