Pheromones are interesting molecules given their ability to evoke changes in the endocrine state and behaviours of animals. In goldfish, a sex pheromone, 17α,20β-dihydroxy-4-pregnen-3-one (17,20β-P), which is released by preovulatory females, is known to trigger the elevation of luteinising hormone (LH) levels, as well as reproductive behaviour in males. Interestingly, when 11-ketotestosterone (11-KT) is implanted into adult female fish, LH levels increase in response to the pheromone at any time of the day, which is normally a male-specific response. However, the neural mechanisms underlying the male-specific information processing of 17,20β-P and its androgen dependence are yet unknown. In the present study, we focused on the preoptic area (POA), which plays important roles in the regulation of reproduction and reproductive behaviours. We mapped activity in the POA evoked by 17,20β-P exposure using the immediate-early gene c-fos. We found that a population of ventral POA neurones close to kisspeptin2 (kiss2) neurones that appear to have important roles in reproduction was activated by 17,20β-P exposure, suggesting that these activated neurones are important for the 17,20β-P response. Next, we investigated the distribution of androgen receptor (ar) in the POA and its relationship with 17,20β-P-responsive and kiss2 neurones. We found that ar is widely expressed in the ventral POA, whereas it is only expressed in approximately 10% of 17,20β-P-activated neurones. On the other hand, it is expressed in almost 90% of the kiss2 neurones. Taken together, it is possible that ar expressing neurones in the ventral POA, most of which were not labelled by c-fos in the present study, may at least partly account for androgen effects on responses to primer pheromones; the ar-positive kiss2 neurones in the ventral POA may be a candidate. These results offer a novel insight into the mechanisms underlying male-specific information processing of 17,20β-P in goldfish.
Keywords: androgen; c-fos; goldfish; preoptic area; sex pheromone.
© 2014 British Society for Neuroendocrinology.