title: On the role of glucocorticoid receptors in brain plasticity.
abstract: 1. The mapping of glucocorticoid receptors (GR) in the rat central nervous system (CNS) has demonstrated their widespread presence in large numbers of nerve and glial cell populations also outside the classical stress regions. 2. The present paper summarizes the evidence that glucocorticoids via GR in the CNS can act as lifelong organizing signals from development to aging. The following examples are given. (a) In the prepubertal and adult offspring, prenatal corticosterone treatment can produce long-lasting changes in striatal dopaminergic communication. (b) In adulthood, the evidence suggests complex regulation by adrenocortical hormones of neurotrophic factors and their receptors in the hippocampal formation. (c) In aging, the strongly GR-immunoreactive pyramidal cell layer of the CA1 hippocampal area appears to be preferentially vulnerable to neurotoxic actions of glucocorticoids, especially in some rat strains. 3. Strong evidence suggests that each nerve cell in the CNS is supported by a trophic unit, consisting of other nerve cells and glial cells, blood vessels, and extracellular matrix molecules. Due to multiple actions on nerve and glial cell populations of the different trophic units, the glucocorticoids may exert either an overall trophic or a neurotoxic action. It seems likely that with increasing age, the endangering actions of glucocorticoids on nerve cells prevail over the neurotrophic ones, leading to reduced nerve cell survival in some trophic units.
authors: Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
authors: K
authors: K
authors: Fuxe
authors: R
authors: R
authors: Diaz
authors: A
authors: A
authors: Cintra
authors: M
authors: M
authors: Bhatnagar
authors: B
authors: B
authors: Tinner
authors: J A
authors: JA
authors: Gustafsson
authors: S O
authors: SO
authors: Ogren
authors: L F
authors: LF
authors: Agnati
mesh_terms: D000305:Adrenal Cortex Hormones / Q000097:blood; D000375:Aging / Q000502:physiology; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001923:Brain Chemistry / Q000502:physiology*; D001931:Brain Mapping; D002470:Cell Survival / Q000502:physiology; D005260:Female; D005346:Fibroblast Growth Factors / Q000378:metabolism; D005938:Glucocorticoids / Q000097:blood; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism; D051381:Rats; D011914:Rats, Inbred BN; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases; D051496:Receptor, Fibroblast Growth Factor, Type 1; D017468:Receptors, Fibroblast Growth Factor / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000032:analysis* / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
chemical_list: D000305:Adrenal Cortex Hormones; D005938:Glucocorticoids; D009479:Neuropeptides; D017468:Receptors, Fibroblast Growth Factor; D011965:Receptors, Glucocorticoid; D005346:Fibroblast Growth Factors; C496350:Fgfr1 protein, rat; D020794:Receptor Protein-Tyrosine Kinases; D051496:Receptor, Fibroblast Growth Factor, Type 1