Abstract
Adolescent social interactions can have long-term effects on physiological responses to stressors in later-life. A larger adolescent group size can result in higher stressor-induced secretion of glucocorticoids in adulthood. The effect may be due to a socially-mediated modulation of gonadal hormones, e.g. testosterone. However, group size (number of animals) has been conflated with social density (space per animal). Therefore it is hard to determine the mechanisms through which adolescent group size can affect the stress response. The current study aimed to tease apart the effects of group size and social density during adolescence on the physiological stress response and gonadal hormone levels in adulthood. Adolescent zebra finches were housed in groups varying in size (2 vs. 5 birds per cage) and density (0.03m3 vs. 0.06m3 per bird) during early adolescence (day 40–60). Density was only manipulated in birds raised in groups of five. Glucocorticoid concentration secreted in response to a standard capture and restraint stressor was quantified in adolescence (day 55±1) and adulthood (day 100+). Basal gonadal hormone concentrations (male testosterone, female estradiol) were also quantified in adulthood. Female birds housed in larger groups, independent of social density, secreted a higher glucocorticoid concentration 45min into restraint regardless of age, and had higher peak glucocorticoid concentration in adulthood. Adult gonadal hormone concentrations were not affected by group size or density. Our results suggest that group size, not density, is a social condition that influences the development of the endocrine response to stressors in female zebra finches, and that these effects persist into adulthood. The findings have clear relevance to the social housing conditions necessary for optimal welfare in captive animals, but also elucidate the role of social rearing conditions in the emergence of responses to stressors that may persist across the lifespan and affect fitness of animals in wild populations.
Highlights
Stressors are unpredictable and uncontrollable stimuli that are perceived to be a threat (Koolhaas et al, 2011), such as being captured (Angelier et al, 2010; Romero and Reed, 2005) or separated from a social group (Hennessey, 1997; RemageHealey et al, 2003)
The interaction was present regardless of age (F6,68 = 1.569, p = 0.170). 15 min into restraint, CORT concentrations of high number/high density (HN/HD) females were significantly lower than those of female birds from all other conditions (LN vs. HN/HD, p = 0.027, d = 0.81; low number (LN)/C vs. HN/HD, p = 0.012, d = 0.99; high number/low density (HN/LD) vs. HN/HD, p = 0.020, d = 0.89). 45 min into restraint, female birds that were housed in larger groups exhibited higher CORT levels than those housed in smaller groups (LN vs. HN/LD, p = 0.014, d = 1.24; LN vs. HN/HD, p = 0.012, d = 1.27; low number/control (LN/C) vs. HN/LD, p = 0.007, d = 1.52; LN/C vs. HN/HD, p = 0.006, d 1.53)
Female birds that were housed in larger groups in early adolescence had a higher peak CORT concentration than that of adult male birds housed in the same way (HN/LD, p = 0.001, d = 1.80; HN/HD, p < 0.001, d = 1.58)
Summary
Stressors are unpredictable and uncontrollable stimuli that are perceived to be a (potential) threat (Koolhaas et al, 2011), such as being captured (Angelier et al, 2010; Romero and Reed, 2005) or separated from a social group (Hennessey, 1997; RemageHealey et al, 2003). An acute rise in GCs is an adaptive strategy to cope with a short-term stressor as the hormones elicit risk-avoidant behaviors (Haller et al, 1998; Rodgers et al, 1999). Repeated or prolonged stress can cause chronic secretion of GCs leading to deleterious effects, such as suppression of reproduction, higher rates of programmed cell death, and immunosuppression (McEwen and Wingfield, 2003; McEwen, 1998; Toufexis et al, 2014). Chronic secretion of stress hormones contributes ‘wear and tear’ to systems affected by GCs, e.g. cardiovascular system (McEwen, 1998; McEwen and Wingfield, 2003), and can induce oxidative stress (Constantini et al, 2011) that may in turn lower survival prospects through higher disease susceptibility, as documented in rats (Rattus norvegicus: Cavigelli and McClintock, 2003; Cavigelli et al, 2009).
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