Plasticity of the reproductive axis caused by social status change in an african cichlid fish: I. Pituitary gonadotropins
Social position in a dominance hierarchy is often tightly coupled with fertility. Consequently,ananimal that can recognize and rapidly take advantage of anopportunity to rise inrankwillhaveareproductive advantage. Reproduction in all vertebrates is controlled by the brain-pituitary-gonad axis,andin males of the African cichlid fish Astatotilapia burtoni, GnRH1 neurons at the apex of this axis are under social control. However, little is known about how quickly social information is transformed into functional reproductive change, or about how socially controlled changes in GnRH1 neurons influence downstream actions of the brain-pituitary-gonad axis. We created an opportunity for reproductively suppressed males to ascend in status and then measured how quickly the perception of this opportunity caused changes in mRNA and protein levels of the pituitary gonadotropins. mRNA levels of the subunits ofLHandFSHrose rapidly in the pituitary30minafter suppressedmalesperceivedanopportunity to ascend. In contrast, mRNA levels of GnRH receptor-1 remained unchanged during social transition butwerehigher in stable dominantcomparedwith subordinate males. In the circulation, levels of both LHand FSH were also quickly elevated. There was a positive correlation betweenmRNAin the pituitary and circulating protein levels for LH and FSH, and both gonadotropins were positively correlated with plasma 11-ketotestosterone. Our results show that the pituitary is stimulated extremely rapidly after perception of social opportunity, probably to allow suppressed males to quickly achieve reproductive success in a dynamic social environment. Copyright © 2010 The Endocrine Society. All rights reserved.
Publication Source (Journal or Book title)
Maruska, K., Levavi-Sivan, B., Biran, J., & Fernald, R. (2011). Plasticity of the reproductive axis caused by social status change in an african cichlid fish: I. Pituitary gonadotropins. Endocrinology, 152 (1), 281-290. https://doi.org/10.1210/en.2010-0875