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Anabolic–androgenic steroids (AAS) increase libido and sexual behavior, but the underlying behavioral mechanisms are unclear. One way AAS may enhance expression of sexual behavior is by increasing the willingness to work for sex. In the present study, sexually-experienced male rats received daily injections of testosterone at supraphysiologic doses (7.5 mg/kg in water with 13% cyclodextrin) or vehicle and were tested for appetitive sexual behavior measured by operant responding for access to an estrous female. Initially, rats were trained in their home cage to respond on a nose-poke under a 10-min fixed-interval schedule for food reward. Once rats achieved stable response rates, the food was replaced by a female, followed by mating for 10 min. There was no effect of testosterone on operant responding for food (28.1 ± 4.4 responses/10 min for testosterone, 30.6 ± 4.3 for vehicle) or sex (35.0 ± 4.0 responses/10 min for testosterone, 37.3 ± 5.2 for vehicle). However, rats made significantly more responses for sex than for food (p < 0.05), and responses for food and sex were positively correlated among individuals (R 2 = 0.6). Additional groups of rats were trained to respond on a lever for the female under a 2nd-order schedule of reinforcement, where 5 responses opened a door to show the female for 5 s. After 15 door openings, the male gained access to the female. There was no effect of testosterone on time to complete 75 responses: 38.4 ± 7.8 min for vehicle controls vs 43.3 ± 6.6 min for testosterone-treated rats (p > 0.05). These findings suggest that chronic high-dose testosterone does not enhance appetitive drive for sexual behavior. [ABSTRACT FROM AUTHOR]

Abstract: The transient actions of gonadal steroids on the adult brain facilitate social behaviors, including reproduction. In male rodents, testosterone acts in the posterior medial amygdala (MeP) and medial preoptic area (MPOA) to promote mating. Adult neurogenesis occurs in both regions. The current study determined if testosterone and/or sexual behavior promote cell proliferation and survival in MeP and MPOA. Two experiments were conducted using the thymidine analog BrdU. First, gonad-intact and castrated male hamsters (n =6/group) were compared 24 h or 7 weeks after BrdU. In MeP, testosterone-stimulated cell proliferation 24 h after BrdU (intact: 22.8±3.9 cells/mm2, castrate: 13.2±1.4 cells/mm2). Testosterone did not promote cell proliferation in MPOA. Seven weeks after BrdU, cell survival was sparse in both regions (MeP: 2.5±0.6 and MPOA: 1.7±0.2 cells/mm2), and was not enhanced by testosterone. In Experiment 2, gonad-intact sexually-experienced animals were mated weekly to determine if regular neural activation enhances cell survival 7 weeks after BrdU in MeP and MPOA. Weekly mating failed to increase cell survival in MeP (8.1±1.6 vs. 9.9±3.2 cells/mm2) or MPOA (3.9±0.7 vs. 3.4±0.3 cells/mm2). Furthermore, mating at the time of BrdU injection did not stimulate cell proliferation in MeP (8.9±1.7 vs. 8.1±1.6 cells/mm2) or MPOA (3.6±0.5 vs. 3.9±0.7 cells/mm2). Taken together, our results demonstrate a limited capacity for neurogenesis in the mating circuitry. Specifically, cell proliferation in MeP and MPOA are differentially influenced by testosterone, and the birth and survival of new cells in either region are not enhanced by reproductive activity. [Copyright &y& Elsevier]