DENSITY-DEPENDENT PRENATAL ANDROGEN EXPOSURE AS AN ENDOGENOUS MECHANISM FOR THE GENERATION OF CYCLES IN SMALL MAMMAL POPULATIONS

Small mammal populations exhibit cyclic fluctuations in their populati on densities. Several hypotheses regarding the mechanisms underlying t hese population cycles have been advanced, but none has yet gained gen eral approval. We propose here an endogenous mechanism based on the ma sculinization of female offspring in response to increased population levels. High population levels trigger the non-specific stress respons e resulting in high levels of circulating androgens in individuals of the population, including pregnant females. These androgens masculiniz e female offspring in utero, thereby reducing the reproductive capacit y of the next generation and subsequently the population size. We have developed and analysed a mathematical model to investigate the possib le role of prenatal androgen exposure in the generation of limit cycle s. We find the locus of Hopf bifurcations for this model and show that limit cycles depend on three parameters: (1) the delay between birth and sexual maturation; (2) the slope of the function that relates aver age prenatal androgen exposure to total population density; and (3) th e difference between the maximum birth rates of the low-and high-andro gen exposed females. We derive the analytical form relating these para meters at the Hopf-bifurcation locus and discuss its biological ramifi cations. In brief, if each of these three parameters is sufficiently l arge, population cycles will result from the endogenous mechanism prop osed. (C) 1998 Academic Press Limited.