Abstract

Steroids modulate the transcription of a multitude of genes and ultimately influence numerous aspects of reproductive behaviors. Our research investigates how one single steroid, testosterone, is able to trigger this vast number of physiological and behavioral responses. Testosterone potency can be changed locally via aromatization into 17β-estradiol which then activates estrogen receptors of the alpha and beta sub-types. We demonstrated that the independent activation of either receptor activates different aspects of male sexual behavior in Japanese quail. In addition, several studies suggest that the specificity of testosterone action on target genes transcription is related to the recruitment of specific steroid receptor coactivators. We demonstrated that the specific down-regulation of the coactivators SRC-1 or SRC-2 in the medial preoptic nucleus by antisense techniques significantly inhibits steroid-dependent male-typical copulatory behavior and the underlying neuroplasticity. In conclusion, our results demonstrate that the interaction between several steroid metabolizing enzymes, steroid receptors and their coactivators plays a key role in the control of steroid-dependent male sexual behavior and the associated neuroplasticity in quail.

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