Maternal Corticosterone Further Reduces the Reproductive Function of Male Offspring Hatched from Eggs Laid by Quail Hens Selected for Exaggerated Adrenocortical Stress Responsiveness

Abstract

Activation of the hypothalamic-pituitary-adrenal (HPA) axis can depress the hypothalamic-pituitary-testicular axis. Male quail cloacal gland (CG) size and foam production shows androgen dependency, and males selected for exaggerated [high stress (HS)] rather than reduced [low stress (LS)] plasma corticosterone (B) stress response exhibit reduced CG and testes development. High stress hens also deposit more B into egg yolks than LS ones, and quail hens given B produce chicks that have a reduced growth rate and adults with heightened HPA responsiveness. Herein, we gave LS and HS hens no B [empty implants, control (CON)] or B-filled implants and assessed the reproductive performances of these hens and their male offspring. Mortality was similarly elevated in LS and HS B-treated hens, but only HS B-implanted hens showed reduced egg production. In male offspring, CG volume (CVOL), intensity of CG foam production (CFP), and the proportion of individuals that produced CG foam were measured from 4 to 11 wk of age. At 6 wk, BW, and at 15 wk, BW, testes weight (TWT), and TWT relative to BW were also determined. Hen treatments did not affect male chick CVOL at 4 wk, but CVOL differed thereafter as follows: LS CON > LS B = HS CON = HS B at 5 and 6 wk and LS CON > LS B > HS CON = HS B from 7 to 11 wk. By 8 wk, and thereafter, CFP differed as follows: LS CON > LS B > HS CON > HS B. Group differences in the proportion of individuals that produced CG foam generally supported CFP findings from 4 to 8 wk of age. Body weight did not differ by treatment at 6 wk of age. By 15 wk, TWT were similarly depressed in both HS groups. However, similarly higher 15-wk BW in the LS-CON and HS-B groups contributed to TWT relative to BW differences as follows: LS-B > LS-CON > HS-B; LS-CON = HS-CON; LS-B > HS-CON; and, HS-CON = HS-B. Both selection for exaggerated HPA responsiveness and maternal B treatment negatively affected the reproductive function of HS male offspring.

Prenatal stress in birds: Pathways, effects, function and perspectives

“…While some studies only collected eggs laid 7 days after the beginning of treatment (de la Cruz et al, 1987;Hayward and Wingfield, 2004) others pooled eggs collected over a longer period (Janczak et al, 2007a-day 5-10;Satterlee et al, 2007-day 7-14; Henriksen et al, submitted for publication-day 12-18; Davis et al, 2008-2-3 weeks). The decision on when to collect eggs might be based on the duration of plasma CORT elevation in each single study, but some studies did not measure plasma CORT in the mothers (Rozenboim et al, 2007;Satterlee et al, 2007;Davis et al, 2008), making it difficult to estimate the duration and intensity of maternal CORT elevation during egg formation. The potential differences in duration and intensity of prenatal exposure to maternal stress due to differences in the experimental design between studies might therefore explain some of the inconsistencies seen between studies regarding the offspring's phenotype.…”

“…Two out of five studies reported a lower hatching mass in offspring of stressed mothers (Love et al, 2005; Henriksen et al, submitted for publication), four out of six studies reported lower body mass later in life (Hayward and Wingfield, 2004;Love et al, 2005; Henriksen et al, submitted for publication; de la Cruz et al, 1987) and none reported an increase in body mass. The two studies that did not find any difference in body mass post hatching between offspring of control and stressed mothers (Janczak et al, 2007a;Satterlee et al, 2007) also did not find any difference in body mass at hatching. Elevated maternal CORT during egg formation therefore seems to have the potential to reduce the prenatal, and especially the postnatal growth of the offspring that hatch from these eggs.…”

“…Studies measuring physiological traits in avian offspring of stressed mothers have mainly looked at different aspects of growth, such as hatching mass (Janczak et al, 2007a;Hayward and Wingfield, 2004;Love et al, 2005;Satterlee et al, 2007; Henriksen et al, submitted for publication), structural size (Love et al, 2005; Henriksen et al, submitted for publication), growth both before (Janczak et al, 2007a;Hayward and Wingfield, 2004;Love et al, 2005; Henriksen et al, submitted for publication) and after sexual maturity (Hayward and Wingfield, 2004;Satterlee et al, 2007), and developmental stability . The latter was assessed by measuring fluctuating asymmetry (FA), believed to be stress-induced deviations from morphological bilateral symmetrical traits (Parsons, 1990;Møller and Swaddle, 1997;Thomson, 1999).…”

“…Immunocompetence was also evaluated in these offspring, either via a T-cell mediated inflammatory response to phytohemagglutinin (PHA, Love et al, 2005) or B-cell mediated production of antibodies during an antigen challenge (sheep red blood cell challenge, Henriksen et al, submitted for publication). The fitness of male offspring has been evaluated by measuring their reproductive function (size and functionality of reproductive organs, Satterlee et al, 2007), while secondary sex ratio has been investigated to see if survival chances differ between the sexes when prenatally exposed to maternal stress (Love et al, 2005). Most of these traits have only been assessed in one or two studies making it impossible to give an indication of how general and consistent the findings are.…”

“…The reduced size and functionality of the reproductive organs (cloacal gland volume and foam production) reported in male quails of mothers with elevated CORT levels (Satterlee et al, 2007), and the lower antibody response in such offspring (see above) might indicate that maternal stress negatively affects the fitness of their male offspring. Consistent with the latter, experimentally elevated maternal CORT levels in female European starlings (Sturnus vulgaris) resulted in a female biased brood at hatching, caused by elevated embryonic mortality in males (Love et al, 2005).…”