Messenger RNA for glial fibrillary acidic protein is decreased in rat brain following acute and chronic corticosterone treatment

Nichols, Nancy R.; Osterburg, Heinz H.; Masters, Jeffrey N.; Millar, Sharon L.; Finch, Caleb E.

doi:10.1016/0169-328x(90)90066-m

Cited by 126 publications

(58 citation statements)

References 15 publications

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“…1A, C) following 8h CORT treatment. In contrast, PLP mRNA levels did not change in response to ADX or CORT as previously observed [28] and are used as the control for RNA concentration for all subsequent experi ments. CR16 RNA is polvadenvlated (not shown) and detected in total RNA from brain and from non-neural tissues including heart, lung and testes but not in kidney, liver or spleen (fig.…”

Section: Resultsmentioning

confidence: 82%

“…The rat proteolipid protein (PLP) RNA was used as a control for input RNA in both the blotting and RNase protection experiments because it does not respond to changes in serum CORT in adult rats [28,29]. The PLP clone used for these experiments was isolated from the hippocampal cDNA library as a nonchanging clone (648-bp insert) and corresponds to the 3'-end of the RNA from nt 2,386 to the poly(A) tail [44].…”

Section: Rna Quantificationmentioning

confidence: 99%

“…Because MR and GR are co localized in hippocampal neurons [10] and can bind and modulate the same promoter sequences [3], a binary glu cocorticoid response model [26] was proposed allowing for dual effects of MR and GR in modulating gene expres sion over a 100-fold range of serum CORT levels found during the circadian cycle and in response to various stressors. The glucocorticoid regulation of the serotonin 5HT1A receptor gene in dentate granule neurons is con sistent with this model in that low CORT suppresses 5HT1A mRNA and high CORT has a greater effect [27], We have previously reported the isolation of glial-specific gene products from a rat hippocampal cDNA library which were regulated by CORT including glial fibrillary acidic protein [28], glycerol phosphate dehydrogenase [29] and transforming growth factor-pi [30], To further pursue our analysis of CORT action in the brain, we now report the isolation of a novel gene whose expression is detected in subsets of neurons including the hippocampus and cortex. This RNA may be predominantly regulated by the MR in the hippocampus.…”

Section: Introductionmentioning

confidence: 99%

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Modulation of a Novel RNA in Brain Neurons by Glucocorticoid and Mineralocorticoid Receptors

Masters

Cotman²,

Osterburg³

et al. 1996

Neuroendocrinology

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A novel cDNA clone, CR16, was isolated from a rat hippocampal cDNA library and characterized for responses to corticosteroids and regional expression. The 4-kb RNA was increased 3-fold by treatment of adrenalectomized (ADX) rats with corticosterone (CORT). Overlapping cDNA totaling 4,374 nt were used to define an open reading frame of 1,356 nt beginning 191 nt from the 5’-end and encoding a 45-kD protein containing 32% proline. CR16 has no obvious homologies to GenBank or protein databases. CR16 RNA was detected by in situ hybridization in neuron-rich layers of the hippocampal formation, layers II, III and VI of the cerebral cortex, thalamus, ventromedial nucleus of the hypothalamus, bed nucleus of the stria terminalis, lateral septal nucleus, nucleus accumbens, olfactory bulb, inferior colliculus, pons and inferior olive. The CR16 RNA has low prevalence in the hippocampus and cortex (<10 pg/µg total RNA) and is elevated 3-fold in both structures in a dose-dependent manner by CORT in ADX rats. Treatment of ADX rats with aldosterone (ALDO), CORT, or RU28362 increased CR16 RNA to similar levels in the hippocampus while ALDO had minimal effects on the level of CR16 RNA relative to CORT or RU28362 in the cortex. Neither shaking stress (2 h) nor 2 h CORT significantly elevated CR16 RNA in the hippocampus, suggesting that its response to elevated CORT is not rapid. ADX lowered CR16 RNA levels by 50% relative to intact rats while low-level CORT replacement (≧4 ng/ml serum CORT) significantly elevated CR16 RNA 2-fold in ADX rats. These results are consistent with both the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) regulating the CR16 gene. This gene will be useful in dissecting the role of MR and GR in CNS neurons.

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Section: Resultsmentioning

confidence: 82%

Section: Rna Quantificationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Modulation of a Novel RNA in Brain Neurons by Glucocorticoid and Mineralocorticoid Receptors

Masters

Cotman²,

Osterburg³

et al. 1996

Neuroendocrinology

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“…Glycocorticoids can reduce the expression and gene synthesis of GFAP in the central nervous system in vivo [7, 8, 29]. Thus, adult rats that underwent adrenalectomy present increased but corticosteroid-reversible levels of messenger RNA for GFAP [30].…”

Section: Discussionmentioning

confidence: 99%

“…However, the effect was reversed when neurons were added to the culture, indicating the importance of astrocyte-neuron interaction in vivo. In astrocytes 2 types of receptor are involved in mediating the response to corticoids, namely mineralocorticoids (type 1) and glycocorticoids (type 2, which mediate GFAP control) [29, 32]. …”

Section: Discussionmentioning

confidence: 99%

Corticosteroids Reduce Glial Fibrillary Acidic Protein Expression in Response to Spinal Cord Injury in a Fetal Rat Model of Dysraphism

Melo-Filho¹,

Barreto²,

Nassr³

et al. 2009

Pediatr Neurosurg

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Background: Exposure of the spinal cord in myelomeningocele (MM) throughout gestation increases spinal injury. Astrocyte activation evidenced by glial fibrillary acidic proteins (GFAP) indicates the extent of injury. Corticosteroids modulate GFAP synthesis, but their effect in MM is unclear. The purpose of this study was to evaluate the GFAP expression in a fetal rat model of dysraphism and the effect of corticosteroid treatment on this marker and on clinical neurological disabilities. Methods: Dysraphism was surgically created in 2 groups of 48 rat fetuses; group 1: control, and group 2: treated with corticosteroid. Each group was subdivided into fetuses with surgically created MM, controls and shams on day 18.5 of gestation (term = 22 days). Fetuses were harvested on day 21.5, examined for evidence of neurological deficits, and the following clinical parameters were registered: kyphosis, tail deformities, leg deformities, leg paralysis or paresis and pain perception. The fetuses were fixed for GFAP immunostaining. Results: All fetuses with MM in group 1 presented neurological deficits and glial reactions with GFAP expression, as opposed to controls and shams. In group 2, corticosteroid treatment prevented some neurological deficits (18–25%), reducing glial response and GFAP expression. Conclusions: Experimentally induced dysraphism in the rat fetus is related to glial response and increased GFAP expression in the spinal cord. Corticoid treatment clinically improved nerve injury in some fetuses. It reduced glial reaction and GFAP expression.

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Steroid metabolism and effects in central and peripheral glial cells

Melcangi¹,

Magnaghi²,

Martini³

1999

J. Neurobiol.

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Hormonal steroids participate in the control of a large number of functions of the central nervous system (CNS); recent data show that they may also intervene at the level of the peripheral nervous system (PNS). Both the CNS and the PNS metabolize endogenous as well as exogenous steroids; one of the major enzymatic system is represented by the 5α‐reductase‐3α–hydroxysteroid complex. This is a versatile system, since every steroid possessing the delta 4‐3keto configuration (e.g., testosterone, progesterone, deoxycorticosterone) may be a substrate. High levels of 5α‐reductase are found in the white matter of the CNS and in purified myelin. The observation that, in addition to neurons, glia may be a target for steroid action is an important recent finding. The effects of progesterone, testosterone, corticoids, and their respective 5α and 3α‐5α derivatives on the expression of glial genes are presented and discussed. It has also been found that progesterone and/or its 5α‐reduced metabolites increase the mRNA for the two major proteins of peripheral myelin, the glycoprotein Po and the peripheral myelin protein 22, in the sciatic nerve of normal and aged animals and in Schwann cells. The hypothesis has been put forward that glycoprotein Po might be under the control of progestagens acting mainly via the progesterone receptor, and that peripheral myelin protein 22 might be controlled via an interaction of steroids with the γ‐aminobutyric acid (GABA)ergic system. It is known that tetrahydroprogesterone, the 3α‐5α–reduced metabolite of progesterone, interacts with the GABAA receptor. Our recent data show that several subunits of this receptor are present in sciatic nerve as well as in Schwann cells that reside in this nerve. These data open multiple possibilities for new therapeutic approaches to demyelinating diseases. © 1999 John Wiley & Sons, Inc. J Neurobiol 40: 471–483, 1999

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Messenger RNA for glial fibrillary acidic protein is decreased in rat brain following acute and chronic corticosterone treatment

Cited by 126 publications

References 15 publications

Modulation of a Novel RNA in Brain Neurons by Glucocorticoid and Mineralocorticoid Receptors

Modulation of a Novel RNA in Brain Neurons by Glucocorticoid and Mineralocorticoid Receptors

Corticosteroids Reduce Glial Fibrillary Acidic Protein Expression in Response to Spinal Cord Injury in a Fetal Rat Model of Dysraphism

Steroid metabolism and effects in central and peripheral glial cells

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