Abstract
A cardinal feature of the reaction to stress is the promotion of energy mobilization, enabling appropriate behavioural responses. Predator odours are naturalistic and ecologically relevant stressors present over evolutionary timescales. In this study, we asked whether maternal predator odour exposure could program long-term energy mobilization in C57BL/6 mice offspring. To test this hypothesis, we measured rates of oxygen consumption in prenatally predator odour exposed mice in adulthood while controlling for levels of locomotor activity at baseline and under stress. Circulating thyroid hormone levels and the transcript abundance of key regulators of the hypothalamic-pituitary-thyroid axis within the periventricular nucleus (PVN) of the hypothalamus and in the liver, including carriers and receptors and thyrotropin-releasing hormone, were measured as endocrine mediators facilitating energy availability. Prenatally predator odour exposed mice of both sexes mobilized more energy during lower energy demand periods of the day and under stressful conditions. Further, prenatally predator odour exposed mice displayed modifications of their hypothalamic-pituitary-thyroid axis through increased circulating thyroxine and thyroid hormone receptor α within the PVN and decreased transthyretin in the liver. Overall, these results suggest that maternal exposure to predator odour is sufficient to increase long-term energy mobilization in adult offspring.
Highlights
A cardinal feature of the response to stress is the promotion of energy mobilization
The hypothalamic-pituitary thyroid (HPT) axis responds to increased energy demands with the release of thyrotropin-releasing hormone (Trh) from the hypothalamus that reaches the pituitary through portal circulation
We previously reported that maternal predator odour exposure in mice and rats alters HPA function in adult offspring, who show increased stress-related behaviors and corticosterone in the context of a stress challenge[12,13]
Summary
A cardinal feature of the response to stress is the promotion of energy mobilization. Studies in the ecology literature have shown that exposures during perinatal life to environmental stressors present during the evolutionary diversification of species lead to adaptive programming of physiological systems involved in energy mobilization to match their predicted environment later in life[3] Some of these physiological changes have been proposed to occur through alterations in hypothalamic-pituitary thyroid (HPT) axis and thyroid hormone function, involving increased circulating thyroid hormone levels as a key mediator of energy requirements in prenatally stressed animals[1,4,5]. Song sparrows and zebra finches exposed to acute corticosterone supplementation mimicking an acute stressor during development, such as an encounter with a predator, display an increase in basal metabolic rate, especially at night during their low activity period[8,9] In these studies, endocrine and gene expression mechanisms associated with these metabolic changes were not examined. Circulating T4 in the blood is bound at 75% to liver-synthesized thyroxine-binding globulin (Tbg) and transthyretin (Ttr) and to albumin (15%)[11]
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