RESUMO
Volatile urinary odors contribute to mate recognition in mice after their detection by the main olfactory epithelium (MOE). We used a habituation/dishabitution task to ask whether the capacity of gonadectomized mice of both sexes to detect and investigate decreasing concentrations of volatile urinary odors from either breeding males or estrous females is modulated by administering androgen or estrogen and if so, whether any effects of these sex steroids are altered by disrupting the sympathetic innervation of the MOE via bilateral superior cervical ganglionectomy (SCGx). In tests given, beginning 51 days after gonadectomy without steroid treatment both male and female subjects detected even the lowest concentrations (1:120 and 1:160 dilutions by volume) of male urinary odors, provided they were SCGx as opposed to sham operated. In subsequent tests given after estradiol benzoate (EB) followed later by 5alpha-dihydrotestosterone (DHT) treatments, neither male nor female subjects detected low concentrations of male urinary odors regardless of whether or not their SCG's were intact. Administration of testosterone (T) prior to a final series of tests restored the ability of gonadectomized subjects of both sexes to detect low concentrations of male urinary odors regardless of their SCG status. This suggests that T, but not its neural metabolites estradiol, or DHT, facilitates responsiveness to low concentrations of male odors in mice of both sexes. In tests given 51 days after gonadectomy without steroid treatment most male and female subjects readily detected the three highest concentrations of estrous female urinary odors whereas SCGx males and females failed to detect the lowest concentrations of these odors. After treatment with EB and then with DHT, gonadectomized mice of both sexes generally failed to detect the three lowest concentrations of estrous female urinary odors regardless of their SCG status. After T treatment; however, subjects of both sexes again detected most dilutions of estrous female urine, provided their SCG's were intact. Again, these results suggest that T, but not estradiol or DHT, facilitates responsiveness to estrous female urinary odors. Provided such an activational effect of T is present, sympathetic, noradrenergic inputs to the MOE may enhance odorant contrast, as previously suggested [Nat. Neurosci. 2 (1999) 106], by reducing the responsiveness of olfactory neurons to low (1:120 and 1:160 dilutions) concentrations of some biologically significant odorants (e.g. male urinary odors) while facilitating their responsiveness to low to moderate (1:80 dilution) concentrations of others (e.g. estrous female urinary odors).