Abstract

AbstractMales and females exhibit innate sex-specific mating behaviors, which are established developmentally. In mammals and birds, phenotypic sex differences in mating behaviors are stable and essentially irreversible, because the underlying neural substrates are irreversibly sex-differentiated prior to puberty due to the effects of gonadal steroids and the sex chromosome complement. In contrast, experimental manipulation of the hormonal milieu of teleost fish in adulthood effectively reverses male and female mating behaviors, illustrating the lifelong sexual lability in their underlying neural substrates. Consistent with this, evidence is accumulating that, in teleosts, both early gonadal steroids and the sex chromosome complement have little effect on the development of sex-typical mating behaviors; instead, recent work in medaka (Oryzias latipes) demonstrates that mutual antagonism between estradiol-17β signaling through an estrogen receptor subtype Esr2b and 11-ketotestosterone signaling through androgen receptor in adulthood, rather than during development, mediates sex-typical mating behaviors in a reversible and transient manner. Further evidence is provided that the pronounced sexual dimorphism and adult steroid-dependent lability in the expression of Esr2b and downstream effectors, including neuropeptide B, in the telencephalic and preoptic nuclei underlie the neural basis of induction, maintenance, and reversal of male and female mating behaviors in teleosts.KeywordsBrainMating behaviorSex steroidSexual spectrumTeleost

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