Testosterone enhances aggression of wild-type mice but not those deficient in type I 5α-reductase

Abstract

Testosterone’s (T) aggression-enhancing effects may be mediated in part by its 5α-reduced, 3-hydroxysteroid dehydrogenized metabolite 5α-androstane-3α,17β-diol (3α-diol). To test this hypothesis, in Expt. 1 gonadectomized (gdx) C21 mice were administered T, 3α-diol, or vehicle and were observed in the resident intruder test of aggression 1 h later. C21 mice administered androgens had significantly higher incidences of aggression than did vehicle-administered mice. In Expt. 2, wild-type mice and mice deficient in the 5α-reductase type I enzyme were administered T or vehicle and tested 1 h later in the resident intruder paradigm. Wild-type mice administered T had significantly shorter latencies and greater incidences of aggression than did 5α-reductase type I knockout mice administered T or vehicle-administered mice. Data from Expt. 1 are consistent with T and 3α-diol having similar aggression-enhancing effects, and results of Expt. 2 suggest that the inability to metabolize T to its 5α-reduced products may attenuate some aggression-enhancing effects of mice in the resident intruder test of aggression.