Steroidogenic properties of isolated adrenocortical cells from Japanese quail selected for high serum corticosterone response to immobilization.

The effect of selection for high stress response on adrenocortical function was examined by measuring the corticosterone response of adrenocortical cells isolated from random-bred Japanese quail and quail selected for high serum corticosterone response to immobilization (high-stress). Highly enriched adrenocortical cells were incubated with various concentrations of ACTH1-24 (ACTH), 8-bromo-cyclic AMP (8Br-cAMP) and pregnenolone for 2 hr. Corticosterone production was measured by radioimmunoassay. Basal corticosterone production values by cells from random-bred and high-stress birds were not different. In contrast, the average maximal ACTH- and 8Br-cAMP-induced corticosterone production by cells from high-stress quail was 89% greater than that of cells from random-bred quail. However, the average pregnenolone-supported corticosterone production by cells from high-stress birds was 34% less than that of cells from random-bred birds. Thus, the data suggest that although random-bred quail cells had a greater potential capacity for corticosterone production, high-stress quail cells had a greater ability to couple ACTH, ACTH-transmembrane-signaling factors and subsequent second messengers with the available steroidogenic enzyme pool. The magnitude of the differences in function between cells from high-stress and random-bred birds was greater for female cells compared to male cells. In addition to differences in cellular function, there were also differences in adrenal and relative adrenal weights between random-bred and high-stress quail. The average, adrenal and relative (mg/100 g body weight) adrenal weights of high-stress quail were 14-16% greater than those of random-bred quail. It is concluded that the enhanced serum corticosterone response of the high-stress quail line is, in part, due to an increase in relative adrenal weight and an increase in adrenocortical cell responsiveness to ACTH.