Progesterone does not inhibit aggression induced by testosterone metabolites in castrated male mice.

Sufficient data exist indicating that testosterone (T) or metabolites of T, i.e., dihydrotestosterone (DHT) and estrogen (E), induce aggressive behavior. The effects of T have also been shown to be suppressed by concurrent administration of progesterone (P). It is unknown if the effects of P are exerted on T directly or upon the T metabolites. The objective of this experiment was to evaluate the inhibitory effects of P on aggression induced by T and T metabolites. Seven male mice were randomly allocated to one of the following treatment groups: castration (C), C + T, C + 5 alpha-dihydrotestosterone (DHT), C + estrogen (E), C + DHT + E (DE), T + P, and DE + P. The males were then placed with androgenized females in three 10-min trials to determine the effects of each treatment on hormone induced aggression. The degree of aggressive behavior displayed was measured by number of trials where attacks occurred (N), mean latency to attack (L), frequency of attacks (AF), duration of attacks (D), and a composite index score (INDEX). All androgen treated groups showed significantly higher degrees of aggression compared to C and T + P animals. P inhibited aggression in T-treated males but did not inhibit aggression in the DE treated group. The data suggest that P inhibits the aggressive effects of T by acting on receptors of the metabolite-producing enzymes or by direct competitive binding for 5 alpha-reductase.

Progestagen effects on elicitation of aggressive behaviour in male mice.

Effects of progesterone on production of androgen-dependent aggression-eliciting pheromones were investigated. Two groups of anosmic (non-fighting) castrated mice treated with testosterone or with testosterone and progesterone, respectively, were attacked to the same degree by intact, isolated (fighting) mice while control mice (castrated only) were attacked less. The findings support the ideas that progesterone may inhibit androgen-induced aggression via a neural and not via a somatic mechanism.

PIP: The effects of progestagen on elicitation of aggressive behavior in male mice were tested. 48 mice were divided as follows: 1) 16 mice used as pheromone testers; 2) 24 mice bilaterally gonadectomized and subcutaneously implanted with either 20 mg testosterone (T), T + progesterone (P), or control beads; and 3) 8 mice sham-castrated and implanted with control beads. 4 days after the beginning of replacement therapy the treated mice were placed on an 18-hour food deprivation schedule in preparation for olfaction tests. A mouse was considered nonaggressive if response was absent (locating a food pellet) within 5 minutes. Zinc sulphate was administered intranasally to produce a peripheral olfactory dysfunction and produce anosmia. P failed to interfere with the actions of T in the production of aggression-eliciting pheromones and in the maintenance of the preputial and seminal vesicle-coagulating glands. Mice which were only castrated were attacked less than either T-treated or T + P-treated mice.