The controlling mechanism for circadian pituitary adrenal periodicity is clearly of central neural origin. Ontogenetic modification of the pituitary adrenal rhythm was investigated in order to determine critical periods in development during which the presence of excess ACTH or corticosteroid would affect normal maturation of the rhythm. Neonatal treatment with ACTH on days 7 to 9 or 17 to 19, but not at other times postnatally, suppressed the circadian plasma corticosteroid rhythm in adult rats. Treatment with corticosterone on day 18, but not on days 3, 6 or 12, had similar persistent effects. Thus, brief exposure to high circulating levels of ACTH or corticosterone during two critical neonatal periods which correspond to specific stages in the development of hypothalamic and forebrain structures may affect the normal development of central structures involved in circadian regulation. Development of the pituitary adrenal rhythm in the female rat is closely related to the onset of puberty. When puberty is delayed, i.e. by neonatal implantation of corticosterone or a sham implant on day 4, maturation of the full amplitude of the circadian rhythm is correspondingly delayed. The role of the hippocampus and septum in the circadian periodicity of stress induced pituitary adrenal responsiveness was investigated. Electrical stimulation of hippocampus in freely behaving chronically implanted adult male rats prolonged the plasma corticosterone response to 10 min restraint stress in the morning, but was without effect in the afternoon. Septal stimulation in the afternoon abolished the plasma corticosterone response to the stress, whereas stimulation in the morning was less effective. These differential effects obtained at the trough and peak of the pituitary adrenal cycle suggest that hippocampus and septum may play a role in producing the diminished stress responsiveness normally observed at the peak of the cycle.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Psychiatry and Mental health
- Biological Psychiatry
- Endocrine and Autonomic Systems