Distribution of corticosteroid receptors in the rhesus brain: Relative absence of glucocorticoid receptors in the hippocampal formation

Citation
Mm. Sanchez et al., Distribution of corticosteroid receptors in the rhesus brain: Relative absence of glucocorticoid receptors in the hippocampal formation, J NEUROSC, 20(12), 2000, pp. 4657-4668
Citations number
85
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE
ISSN journal
02706474 → ACNP
Volume
20
Issue
12
Year of publication
2000
Pages
4657 - 4668
Database
ISI
SICI code
0270-6474(20000615)20:12<4657:DOCRIT>2.0.ZU;2-1
Abstract
Chronic stress has been associated with degenerative changes in the rodent and primate hippocampus, presumably mediated in part via neuronal glucocort icoid receptors (GRs). In the rat brain, GRs are widely distributed and are particularly dense in the hippocampus. The distribution of GRs in the prim ate brain, however, has not been fully characterized. In this study, we use d in situ hybridization histochemistry and immunohistochemistry to map the distribution of GR mRNA and GR protein, respectively, in adult rhesus monke ys (Macaca mulatta). In contrast to its well established distribution in th e rat brain, GR mRNA was only weakly detected in the dentate gyrus (DG) and Cornu Ammonis (CA) of the macaque hippocampus, whereas it was abundant in the pituitary (PIT), cerebellum (CBL), hypothalamic paraventricular nucleus (PVN), and, to a lesser extent, the neocortex. Immunohistochemical stainin g indicated a very low density of GR-like immunoreactive cells within the m acaque hippocampal formation in contrast to the high density observed withi n the PVN, prefrontal and entorhinal cortices, and cerebellar cortex. Relat ive to the low level of GR, mineralocorticoid receptor (MR) mRNA and protei n expression were abundant within the DG and CA of the rhesus monkey hippoc ampal formation. These results indicate that, in the primate, neocortical a nd hypothalamic areas may be more important targets for GR-mediated effects of glucocorticoids than the hippocampus. Alternatively, it is also possibl e that glucocorticoid effects are mediated through the MRs present in the h ippocampal formation.