Meeting Abstract
Envisioning the stereotype of human masculinity – chest puffing, competing, boasting of sexual prowess – we may be inclined to attribute such behavior to Testosterone. However, studies in a range of vertebrate species continue to demonstrate that estrogens are the predominant steroid hormone regulating male sexual behavior. More specifically, the neural conversion of testosterone into 17β-Estradiol (E2) via the aromatase enzyme is the critical step required to initiate such behaviors. Since aromatase activity (AA) can be rapidly altered, the time scale in which local E2 in the brain can be changed is predicted to relate to its fast, non-genomic effects on behavior. Focusing on the medial preoptic nuclei (POM), a region in the hypothalamus shown to regulate male sexual behavior, Japanese quail (Coturnix japonica) show rapid changes in AA follow both brief sexual interaction (5 min) and acute stress (15 min restraint). The directionality of these changes, however, seem counterintuitive – sexual interaction results in decreased AA in the POM while acute stress results in a increase in AA. Follow-up studies suggested that E2 regulation may be more complicated than simply using AA as a proxy for E2 changes. Measurements of E2 in the brain tissue (isolated POM) show a similar, but minor, decrease in E2 following sexual interaction, but the same measurement following acute stress show a strong decrease (in contradiction to the AA directionality). This decrease following stress suggests that local E2 regulation during or following stress may involve a catabolic pathway not yet fully characterized. These data highlight the complexity of rapid control of neurosteroid concentrations while opening additional questions concerning the regulation and role of these changes in stress conditions.
