Hypercortisolism among socially subordinate wild baboons originates at the CNS level
R. M. Sapolsky
Department of Biological Sciences, Stanford University, CA 94305.
Recent studies suggest that the hypercortisolism and dexamathasone
resistance of depression arise, at least in part, at the level of the
brain, ie, cortisol-releasing factor (CRF) and/or other
corticotropin-secretagogues are hypersecreted. This article suggests a
similar cause of the hypercortisolism of social subordinance. Two troops of
wild olive baboons, living freely in the Serengeti Ecosystem of East
Africa, have been under long-term study. Consistently, in stable dominance
hierachies, subordinate males are hypercortisolemic relative to dominant
animals. Furthermore, hypercortisolemic males are dexamethasone resistant.
There are no rank-related difference in cortisol clearance or adrenal
sensitivity to corticotropin, suggesting a pituitary and/or neural locus of
the hypercortisolism. Subordinate males were shown to secrete less
corticotropin in response to a CRF-challenge than did dominant males.
Following the logic used in similar studies with depressives, if
subordinate males were hypercortisolemic despite decreased pituitary
sensitivity to CRF, then this implies that the hyperactivity of the
adrenocortical axis is driven at the level of the brain. Furthermore,
subordinate males were hyporesponsive to CRF after administration of
metyrapone, which blocks cortisol secretion and disinhibits the pituitary
from feedback inhibition. Thus, the pituitary appears to have lost
sensitivity to CRF itself in these low-ranking males. These observations
are interpreted in light of behavioral data suggesting that these
subordinate males are under sustained social stress.
