Aromatization mediates aggressive behavior in quail.
Although testosterone (T) stimulates aggressive and reproductive behaviors in males of many vertebrate species, it is now known that the full expression of T action in the brain requires aromatization to estradiol (E2) and subsequent interaction of locally formed E2 with nuclear estrogen receptors. In experiments reported here, we used a behavioral test which quantifies the response of an individual male Japanese quail (Coturnix coturnix japonica) to the visual stimulus of a conspecific. We have called this behavior aggression because it shares many features in common with traditional measures of aggression, e.g., predicting dominance and subordinance. Nevertheless, the behavior probably also combines a complex steroid-sensitive masculine behavior. The advantage of this test is that it allows the discrimination of individual differences in masculine behavior but avoids fighting and sexual encounters per se, thereby reducing effects of learning, a problem with previous tests of avian aggression. In addition, this test has been applied usefully to identify neuroendocrine correlates to male behavior. Using this test, the arousal of reproductively inactive males (hereafter referred to as aggression) is activated by administration of T or estradiol benzoate (EB), but not by 5 alpha-dihydrotestosterone (DHT). T-induced aggression was blocked by the aromatase inhibitor 4-hydroxyandrostenedione (OHA), an effect partially reversed by treatment with EB. In addition, OHA or the estrogen receptor blocker CI-628 reduced aggressiveness of reproductively active males whereas the androgen receptor blocker flutamide had no effect. Results with the 5 alpha-reductase inhibitor N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 alpha-carboxyamide (4-MA) were equivocal. Additionally, treatment of reproductively inactive quail with T or E2 but not DHT increased aromatase activity in the hypothalamus-preoptic area (HPOA). We conclude, therefore, that T to E2 conversion is essential for the activation of aggressiveness in this species. Although locally formed estrogen exerts its effects on aggression in part by increasing activity of aromatase per se, analysis of the time course of behavioral induction or suppression by the various treatments suggests that the response has multiple components, including both short latency, receptor-independent and long latency, receptor-dependent events.
Schlinger
B A
BA
Department of Psychology, University of California, Los Angeles 90024.
Callard
G V
GV
D058891:5-alpha Reductase Inhibitors; D000374:Aggression / Q000187:drug effects / Q000502:physiology*; D000735:Androstenedione / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D047072:Aromatase Inhibitors; D001378:Azasteroids / Q000494:pharmacology; D001522:Behavior, Animal / Q000502:physiology*; D003370:Coturnix / Q000502:physiology*; D013196:Dihydrotestosterone / Q000031:analogs & derivatives / Q000494:pharmacology; D004958:Estradiol / Q000378:metabolism / Q000494:pharmacology*; D005260:Female; D005485:Flutamide / Q000494:pharmacology; D007031:Hypothalamus / Q000201:enzymology; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D009594:Nitromifene / Q000494:pharmacology; D011301:Preoptic Area / Q000201:enzymology; D011784:Quail / Q000502:physiology*; D013739:Testosterone / Q000378:metabolism / Q000494:pharmacology*
D058891:5-alpha Reductase Inhibitors; D047072:Aromatase Inhibitors; D001378:Azasteroids; D013196:Dihydrotestosterone; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D009594:Nitromifene; C031563:17-N,N-diethylcarbamoyl-4-methyl-4-azaandrostane-3-one; D005485:Flutamide; D001141:Aromatase; C014594:formestane