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Can Predators Regulate Small Mammal Populations? Evidence from House Mouse Outbreaks in Australia
A. R. E. Sinclair, Penny D. Olsen and T. D. Redhead
Vol. 59, No. 3 (Dec., 1990), pp. 382-392
Stable URL: http://www.jstor.org/stable/3545150
Page Count: 11
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House mouse Mus domesticus populations in Australia can occur at either low or very high densities. During a 2-yr study mice increased from rarity to abundance in two phases: in phase A mice reached medium densities and declined, in phase B they reached very high densities before declining to near extinction. We hypothesise that mice were regulated by predators in phase A, but escaped from regulation to form plagues in phase B. We measured directly the mortality imposed by raptors and mammalian predators. Two predictions were tested: (1) if predators regulate prey populations then the predator total response should be density-dependent within the range of low densities (phase A); (2) when a prey outbreak occurs (phase B) predator total response should be inversely density-dependent. From counts of raptors, mouse remains in raptor pellets and in mammalian scats, the functional and numerical responses of raptors and mammalian predators were measured. The product of these two responses allowed an estimate of the predator total response, and, therefore, a test of the two predictions from the predator regulation hypothesis. Both predictions were corroborated by the results. The impact of predators at lower prey densities (phase A) was density-dependent. At higher densities (phase B) total predator response was inversely density-dependent and predators were unable to regulate the mouse population. The functional response curve increased linearly at lower densities and indicated a constant predation rate without satiation. At higher densities predators ate a similar amount regardless of density and appeared to be satiated. The main density-dependent effect was derived from the numerical response; at lower mouse densities raptor numbers increased proportionally with density, but remained constant and at lower numbers when mice were at higher densities. Predation of female mice was density dependent in phase A, but that of males was density-independent. At low mouse densities (phase A), two factors, predation and disease, seemed to act on the mouse population, each independently of the other. Their additive effect may have regulated the mouse population in phase A, but failed to do so in phase B.
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