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On the role of glucocorticoid receptors in brain plasticity (1996)

Fuxe, Kjell ; Diaz, Rochellys ; Cintra, Antonio ; [et al.]

Springer

Cellular and molecular neurobiology 16 (1996), S. 239-258

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ISSN: 1573-6830

Keywords: glucocorticoid receptors ; brain ; development ; development ; adulthood ; aging ; neurotrophic factors ; dopamine ; neurons ; astroglia

Source: Springer Online Journal Archives 1860-2000

Topics: Biology

Notes: Summary 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.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF02088179

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Suppression of protein kinase C and the stimulation of glucocorticoid receptor synthesis by dexamethasone in human fibroblasts derived from tumor tissue (1990)

Gadson, Preston ; McCoy, Judy ; Wikström, Ann Charlotte ; [et al.]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 43 (1990), S. 185-198

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ISSN: 0730-2312

Keywords: protein kinase C ; glucocorticoid ; dexamethasone ; fibroblast ; tumor tissue ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Exposure of fibroblasts derived from keloid tissues, desmoid and dermal tissue from individuals with Gardner's syndrome -(GS) to dexamethasone resulted in the suppression of protein kinase C -(PKC) activity and [3H] thymidine incorporation into DNA, and a 20°fold induction of glutamine synthetase activity. Treatment of GS and keloid fibroblasts with 0.1 μM dexamethasone for 36 h increased glucocorticoid receptor -(GR) synthesis, as determined by [35S] methionine labeling and immunoprecipitation with a monoclonal antibody to the human GR. The suppression of PKC activity by dexmethasone was shown to result from a loss of protein mass as determined by immunoblotting using an antibody to PKC type III. In contrast to these results, exposure of fibroblasts isolated from normal tissues to dexamethasone did not result in the suppression PKC and [3H]thymidine incorporation, there was only a sixfold induction of glutamine synthetase, and a decrease of GR synthesis. As no primary receptor binding defect could be detected, the altered response of tumor cells to steroid-occupied receptor indicates a partial post-receptor binding defect in GS and keloid cells.

Additional Material: 5 Ill.