Endocrine Abstracts

Animals that are socially isolated for extended periods show behavioural and physiological changes, including alterations in hypothalamo-pituitary-adrenocortical (HPA) activity. However, there is conflicting data regarding the effects of social isolation on the HPA axis, with studies indicating increased¹, decreased² and unchanged³ corticosterone levels following social isolation. We investigated the effects of social isolation on HPA activity and on tissue sensitivity to glucocorticoids.

Male Sprague–Dawley rats (n=20) were initially group housed (5 per cage), and then randomly assigned to one of two social conditions. Ten rats were housed as isolates and the other 10 rats were housed in two groups of five for a period of one week. Both socially isolated and group housed rats were then either exposed to an acute restraint stress (t=15 min) or left undisturbed before blood samples were collected to determine plasma ACTH. Pituitary, hypothalamic and hippocampal tissue samples were collected for western blot analysis to detect expression of the glucocorticoid-inducible protein, annexin-1 and pituitary tissue was cultured in vitro culture and pituitary sensitivity to CRH was determined.

Social isolation had no significant effect on weight gain or basal plasma ACTH compared to controls. Social isolation induced a reduced expression of annexin-1 in the pituitary and hippocampus compared to group housed controls. Acute restraint stress induced an increase in pituitary annexin-1 levels in group housed animals, but failed to influence pituitary annexin-1 levels in social isolates. Furthermore, in social isolates the pituitary ACTH response to CRH stimulation was significantly increased compared to group housed controls.

These results suggest that social isolation leads to impaired glucocorticoid negative feedback and increased pituitary sensitivity to CRH. These findings suggest that social isolation induces a stress hyper-responsive phenotype.

References

1. Sandstrom et al. 2005 Behav Brain Res 156 289–296.

2. Sanchez et al. 1998 Endocrinology 139 579–587.

3. Haller et al. 1999 Psychopharmacology 144 311–315.