The risk of predation can cause strong antipredator behaviors and marked stressinduced changes in physiology. In mothers, predator-induced stress can reduce reproductive fitness and alter offspring phenotypes. Acting via these generational, maternal stress effects, predation risk may continue to influence the demography of prey populations even when the predators are no longer present. The 10-year snowshoe hare cycle is the classic top-down predator-driven example in nature and is caused both by direct mortality and by indirect risk effects. During the decline phase, virtually, all hares die because they are killed and simultaneously hares exhibit pronounced stress effects caused by high predation risk. However, the rapidity of the decline phase varies among cycles. When the decline is extremely rapid, we expect that the risk experienced by hares is much greater than when the decline is prolonged. The enigma of these cycles is the low phase following the decline, when there is little or no population growth in spite of the absence of predators and ample food. Previously, we have shown that predator-induced maternal stress decreases reproduction and compromises the offspring stress axis. Here, we examine how the severity of predation risk during six separate population declines is related to the length of the subsequent low phase. We show that the more severe the decline, as indicated by the greater rate of loss of hares, the longer the subsequent low phase. These results support the hypothesis that the greater the degree of risk, the longer the generational impact on population demography (the longer the low phase of the hare population). Our findings have broad applicability to conservation and management efforts; even when a stressor (predator, human disturbance) is removed or when exposure may be short term (drought, fire or translocation), the signature of the stressor may be evident over several future generations.

Chronic stressors, such as chronic isolation in social mammals, can elevate glucocorticoids, which can affect cellular mechanisms of aging, including increased levels of oxidative stress and shortened telomere lengths. Recent work in the selectively social prairie vole ( Microtus ochrogaster ) suggests that oxytocin and social support may mitigate some of the negative consequences of social isolation, possibly by reducing glucocorticoid levels. We investigated the influences of isolation, social support, and daily oxytocin injections in female prairie voles. Glucocorticoid levels, oxidative damage, telomere length, and anhedonia, a behavioral index of depression, were measured throughout the study. We found that six weeks of chronic isolation led to increased glucocorticoid levels, oxidative damage, telomere degradation and anhedonia. However, daily oxytocin injections in isolated voles prevented these negative consequences. These findings demonstrate that chronic social isolation in female prairie voles is a potent stressor that results in depression-like behavior and accelerated cellular aging. Importantly, oxytocin can completely prevent the negative consequences of social isolation.

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Animal behaviour research has experienced a renewed interest in consistent individual differences (i.e. animal personality or temperament). Recent ecological studies have identified environmental conditions that give rise to the development and evolution of temperaments and to fitness-related outcomes of temperament. Additional literature has also described relationships between temperaments and physiological regulation. However, one-to-one relationships between one behavioural trait and one physiological system do not account for co-selection of behavioural and physiological traits, nor the complex signalling among physiological systems. In the current paper, we review the literature on multiple physiological processes associated with temperament, propose temperament-specific physiological profiles, and focus on next steps to understand the functional significance, evolution and maintenance of temperaments. We propose that to understand causes and consequences of temperament we need to characterize integrative physiological profiles associated with different temperaments.