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Journal of Neuroscience, Vol 11, 3695-3704, Copyright © 1991 by Society for Neuroscience
Inhibition of glucocorticoid secretion by the hippocampal formation in the primate
RM Sapolsky, S Zola-Morgan and LR Squire
Department of Biological Sciences, Stanford University, California 94305.
Inhibition of the adrenocortical axis by glucocorticoids (GCs) occurs at
both hypothalamic and suprahypothalamic sites. In the rat, the hippocampus
has been shown to be an essential suprahypothalamic site. The present study
shows that the hippocampal system serves a similar role in the nonhuman
primate. Bilateral lesions that included the hippocampal formation and the
parahippocampal cortex; the hippocampal formation, parahippocampal cortex,
and the amygdala; or the fornix all produced GC hypersecretion in
cynomolgus monkeys. The hypersecretion occurred throughout the day.
Moreover, these lesions were also associated with dexamethasone resistance
(i.e., GC hypersecretion following administration of the synthetic GC
dexamethasone). The hypersecretion could not be attributed to acute
surgical trauma, because neither circumscribed lesions of the amygdala nor
conjoint lesions of the perirhinal and parahippocampal cortex produced
adrenocortical abnormalities. Finally, in agreement with data derived from
the rat, the GC hypersecretion following hippocampal lesions was transient.
Secretory activity returned to normal levels by 6-15 months in all operated
groups. Thus, the primate hippocampal system appears to share some
neuroendocrine functions with the rodent.
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