Ontogeny of Glucocorticoid Binding in Rodent Brain

Abstract

Neonatal treatment with corticosterone can differentially and persistently reduce either the basal level of plasma corticosterone or the amplitude of the adult diurnal rhythm in the rat depending on the age at which exposure to the steroid occurs. This alteration of basal secretion by hormonal manipulation during the first postnatal week may be related to the high levels of corticosterone found in pituitary cell nuclei following exposure of the immature rat to exogenous corticoid. The ontogenetic course of cytosol binding in the pituitary suggests a mechanism by which such vulnerability may occur. The hypothalamus was the only brain region found to have a constant level of cell nuclear binding throughout development, although it closely resembles the brain as a whole with regard to the development of cytosol binding sites. The significant postnatal neurogenesis of the hippocampus is reflected in a large postnatal rise in both cytosol and nuclear binding of corticosterone. This increase would appear to be due in part to a delay in binding competence by the pyramidal and granule cells of the hippocampus. The autoradiographic evidence indicates that in the immature rat the retention of steroid by hippocampal pyramidal cells correlates directly with the embryonic age of the neuron. Likewise, the oldest granule cells are the most heavily labelled granule cells in the dentate gyrus, while newly arrived cells do not concentrate corticosterone. This would suggest that an event in cellular differentiation occurs sometime after the cells are “in position,” which permits the binding of glucocorticoids by these hippocampal neurons.