Postmortem decay in glucocorticoid binding in human and primate brain.
Numerous studies of glucorticoid receptors in the rodent brain suggest that similar studies of normal or diseased human brains might be informative. However, a major confound in quantification of such receptors is their possible decay during the lagtime between death and autopsy. We find evidence for such decay. Assay conditions were optimized in a number of ways to remove endogenous glucocorticoids occupying receptors at the time of death. Despite this, [3H]dexamethasone binding in 3-4.5 h postmortem human hippocampus was approximately half that of fresh human primate tissue, while no binding was detectable in 12-24 h postmortem material. In support of the idea of postmortem decay of these receptors, binding in slices of primate temporal cortex left at room temperature declined approximately 50% by 6 h postmortem.
Sapolsky
R M
RM
Department of Biological Sciences, Stanford University, CA 94305.
Meaney
M J
MJ
D000818:Animals; D002522:Chlorocebus aethiops; D003907:Dexamethasone / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008254:Macaca nemestrina; D008297:Male; D011180:Postmortem Changes; D011965:Receptors, Glucocorticoid / Q000378:metabolism*
D011965:Receptors, Glucocorticoid; D003907:Dexamethasone