Postmortem decay in glucocorticoid binding in human and primate brain

Brain Res. 1988 May 10;448(1):182-5. doi: 10.1016/0006-8993(88)91117-1.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chlorocebus aethiops
  • Dexamethasone / metabolism
  • Hippocampus / metabolism*
  • Hippocampus / pathology
  • Humans
  • Macaca nemestrina
  • Male
  • Postmortem Changes*
  • Receptors, Glucocorticoid / metabolism*

Substances

  • Receptors, Glucocorticoid
  • Dexamethasone