Density-dependent prenatal androgen exposure as an endogenous mechanism for the generation of cycles in small mammal populations

Lindsay G. Cowell, Larry B. Crowder, Thomas B. Kepler

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Small mammal populations exhibit cyclic fluctuations in their population densities. Several hypotheses regarding the mechanisms underlying these population cycles have been advanced, but none has yet gained general approval. We propose here an endogenous mechanism based on the masculinization of female offspring in response to increased population levels. High population levels trigger the non-specific stress response resulting in high levels of circulating androgens in individuals of the population, including pregnant females. These androgens masculinize female offspring in utero, thereby reducing the reproductive capacity of the next generation and subsequently the population size. We have developed and analysed a mathematical model to investigate the possible role of prenatal androgen exposure in the generation of limit cycles. 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 average prenatal androgen exposure to total population density; and (3) the difference between the maximum birth rates of the low- and high-androgen exposed females. We derive the analytical form relating these parameters at the Hopf-bifurcation locus and discuss its biological ramifications. In brief, if each of these three parameters is sufficiently large, population cycles will result from the endogenous mechanism proposed.

Original languageEnglish (US)
Pages (from-to)93-106
Number of pages14
JournalJournal of Theoretical Biology
Volume190
Issue number1
DOIs
StatePublished - Jan 7 1998

Fingerprint

Mammals
androgens
small mammals
Androgens
Cycle
Dependent
Population Density
Population
Hopf bifurcation
population density
Limit Cycle
Hopf Bifurcation
masculinization
Locus
Sexual Maturation
loci
birth rate
Birth Rate
stress response
reproductive performance

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Density-dependent prenatal androgen exposure as an endogenous mechanism for the generation of cycles in small mammal populations. / Cowell, Lindsay G.; Crowder, Larry B.; Kepler, Thomas B.

In: Journal of Theoretical Biology, Vol. 190, No. 1, 07.01.1998, p. 93-106.

Research output: Contribution to journalArticle

@article{eb8bd57bf2e14b49b0181bdedd453e1e,
title = "Density-dependent prenatal androgen exposure as an endogenous mechanism for the generation of cycles in small mammal populations",
abstract = "Small mammal populations exhibit cyclic fluctuations in their population densities. Several hypotheses regarding the mechanisms underlying these population cycles have been advanced, but none has yet gained general approval. We propose here an endogenous mechanism based on the masculinization of female offspring in response to increased population levels. High population levels trigger the non-specific stress response resulting in high levels of circulating androgens in individuals of the population, including pregnant females. These androgens masculinize female offspring in utero, thereby reducing the reproductive capacity of the next generation and subsequently the population size. We have developed and analysed a mathematical model to investigate the possible role of prenatal androgen exposure in the generation of limit cycles. 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 average prenatal androgen exposure to total population density; and (3) the difference between the maximum birth rates of the low- and high-androgen exposed females. We derive the analytical form relating these parameters at the Hopf-bifurcation locus and discuss its biological ramifications. In brief, if each of these three parameters is sufficiently large, population cycles will result from the endogenous mechanism proposed.",
author = "Cowell, {Lindsay G.} and Crowder, {Larry B.} and Kepler, {Thomas B.}",
year = "1998",
month = "1",
day = "7",
doi = "10.1006/jtbi.1997.0543",
language = "English (US)",
volume = "190",
pages = "93--106",
journal = "Journal of Theoretical Biology",
issn = "0022-5193",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Density-dependent prenatal androgen exposure as an endogenous mechanism for the generation of cycles in small mammal populations

AU - Cowell, Lindsay G.

AU - Crowder, Larry B.

AU - Kepler, Thomas B.

PY - 1998/1/7

Y1 - 1998/1/7

N2 - Small mammal populations exhibit cyclic fluctuations in their population densities. Several hypotheses regarding the mechanisms underlying these population cycles have been advanced, but none has yet gained general approval. We propose here an endogenous mechanism based on the masculinization of female offspring in response to increased population levels. High population levels trigger the non-specific stress response resulting in high levels of circulating androgens in individuals of the population, including pregnant females. These androgens masculinize female offspring in utero, thereby reducing the reproductive capacity of the next generation and subsequently the population size. We have developed and analysed a mathematical model to investigate the possible role of prenatal androgen exposure in the generation of limit cycles. 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 average prenatal androgen exposure to total population density; and (3) the difference between the maximum birth rates of the low- and high-androgen exposed females. We derive the analytical form relating these parameters at the Hopf-bifurcation locus and discuss its biological ramifications. In brief, if each of these three parameters is sufficiently large, population cycles will result from the endogenous mechanism proposed.

AB - Small mammal populations exhibit cyclic fluctuations in their population densities. Several hypotheses regarding the mechanisms underlying these population cycles have been advanced, but none has yet gained general approval. We propose here an endogenous mechanism based on the masculinization of female offspring in response to increased population levels. High population levels trigger the non-specific stress response resulting in high levels of circulating androgens in individuals of the population, including pregnant females. These androgens masculinize female offspring in utero, thereby reducing the reproductive capacity of the next generation and subsequently the population size. We have developed and analysed a mathematical model to investigate the possible role of prenatal androgen exposure in the generation of limit cycles. 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 average prenatal androgen exposure to total population density; and (3) the difference between the maximum birth rates of the low- and high-androgen exposed females. We derive the analytical form relating these parameters at the Hopf-bifurcation locus and discuss its biological ramifications. In brief, if each of these three parameters is sufficiently large, population cycles will result from the endogenous mechanism proposed.

UR - http://www.scopus.com/inward/record.url?scp=0032491862&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032491862&partnerID=8YFLogxK

U2 - 10.1006/jtbi.1997.0543

DO - 10.1006/jtbi.1997.0543

M3 - Article

C2 - 9473394

AN - SCOPUS:0032491862

VL - 190

SP - 93

EP - 106

JO - Journal of Theoretical Biology

JF - Journal of Theoretical Biology

SN - 0022-5193

IS - 1

ER -