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Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus

BACKGROUND: Reactive gliosis has the potential to alter biomechanical properties of the brain, impede neuronal regeneration and affect plasticity. Determining the onset and progression of reactive astrogliosis and microgliosis due to hydrocephalus is important for designing better clinical treatment...

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Autores principales: Miller, Janet M, McAllister II, James P
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1899521/
https://www.ncbi.nlm.nih.gov/pubmed/17555588
http://dx.doi.org/10.1186/1743-8454-4-5
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author Miller, Janet M
McAllister II, James P
author_facet Miller, Janet M
McAllister II, James P
author_sort Miller, Janet M
collection PubMed
description BACKGROUND: Reactive gliosis has the potential to alter biomechanical properties of the brain, impede neuronal regeneration and affect plasticity. Determining the onset and progression of reactive astrogliosis and microgliosis due to hydrocephalus is important for designing better clinical treatments. METHODS: Reactive astrogliosis and microgliosis were evaluated as the severity of hydrocephalus increased with age in hydrocephalic H-Tx rats and control littermates. Previous studies have suggested that gliosis may persist after short-term drainage (shunt treatment) of the cerebrospinal fluid. Therefore shunts were placed in 15d hydrocephalic rats that were sacrificed after 6d (21d of age) or after 21d (36d of age). Tissue was processed for Western blot procedures and immunohistochemistry, and probed for the astrocytic protein, Glial Fibrillary Acidic Protein (GFAP) and for microglial protein, Isolectin B4 (ILB4). RESULTS: In the parietal cortex of untreated hydrocephalic animals, GFAP levels increased significantly at 5d and at 12d compared to age-matched control rats. There was a continued increase in GFAP levels over control at 21d and at 36d. Shunting prevented some of the increase in GFAP levels in the parietal cortex. In the occipital cortex of untreated hydrocephalic animals, there was a significant increase over control in levels of GFAP at 5d. This trend continued in the 12d animals, although not significantly. Significant increases in GFAP levels were present in 21d and in 36d animals. Shunting significantly reduced GFAP levels in the 36d shunted group. Quantitative grading of immuno-stained sections showed similar changes in GFAP stained astrocytes. Immuno-stained microglia were altered in shape in hydrocephalic animals. At 5d and 12d, they appeared to be developmentally delayed with a lack of processes. Older 21d and 36d hydrocephalic animals exhibited the characteristics of activated microglia, with thicker processes and enlarged cell bodies. Following shunting, fewer activated microglia were present. Histologic examination of the periventricular area and the periaqueductal area showed similar findings with the 21d and 36d animals having increased populations of both astrocytes and microglia which were reduced following shunting with a more dramatic reduction in the long term shunted animals. CONCLUSION: Overall, these results suggest that reactive astrocytosis and microgliosis are associated with progressive untreated ventriculomegaly, but that shunt treatment can reduce the gliosis occurring with hydrocephalus.
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spelling pubmed-18995212007-06-27 Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus Miller, Janet M McAllister II, James P Cerebrospinal Fluid Res Research BACKGROUND: Reactive gliosis has the potential to alter biomechanical properties of the brain, impede neuronal regeneration and affect plasticity. Determining the onset and progression of reactive astrogliosis and microgliosis due to hydrocephalus is important for designing better clinical treatments. METHODS: Reactive astrogliosis and microgliosis were evaluated as the severity of hydrocephalus increased with age in hydrocephalic H-Tx rats and control littermates. Previous studies have suggested that gliosis may persist after short-term drainage (shunt treatment) of the cerebrospinal fluid. Therefore shunts were placed in 15d hydrocephalic rats that were sacrificed after 6d (21d of age) or after 21d (36d of age). Tissue was processed for Western blot procedures and immunohistochemistry, and probed for the astrocytic protein, Glial Fibrillary Acidic Protein (GFAP) and for microglial protein, Isolectin B4 (ILB4). RESULTS: In the parietal cortex of untreated hydrocephalic animals, GFAP levels increased significantly at 5d and at 12d compared to age-matched control rats. There was a continued increase in GFAP levels over control at 21d and at 36d. Shunting prevented some of the increase in GFAP levels in the parietal cortex. In the occipital cortex of untreated hydrocephalic animals, there was a significant increase over control in levels of GFAP at 5d. This trend continued in the 12d animals, although not significantly. Significant increases in GFAP levels were present in 21d and in 36d animals. Shunting significantly reduced GFAP levels in the 36d shunted group. Quantitative grading of immuno-stained sections showed similar changes in GFAP stained astrocytes. Immuno-stained microglia were altered in shape in hydrocephalic animals. At 5d and 12d, they appeared to be developmentally delayed with a lack of processes. Older 21d and 36d hydrocephalic animals exhibited the characteristics of activated microglia, with thicker processes and enlarged cell bodies. Following shunting, fewer activated microglia were present. Histologic examination of the periventricular area and the periaqueductal area showed similar findings with the 21d and 36d animals having increased populations of both astrocytes and microglia which were reduced following shunting with a more dramatic reduction in the long term shunted animals. CONCLUSION: Overall, these results suggest that reactive astrocytosis and microgliosis are associated with progressive untreated ventriculomegaly, but that shunt treatment can reduce the gliosis occurring with hydrocephalus. BioMed Central 2007-06-07 /pmc/articles/PMC1899521/ /pubmed/17555588 http://dx.doi.org/10.1186/1743-8454-4-5 Text en Copyright © 2007 Miller and McAllister II; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Miller, Janet M
McAllister II, James P
Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title_full Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title_fullStr Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title_full_unstemmed Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title_short Reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
title_sort reduction of astrogliosis and microgliosis by cerebrospinal fluid shunting in experimental hydrocephalus
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1899521/
https://www.ncbi.nlm.nih.gov/pubmed/17555588
http://dx.doi.org/10.1186/1743-8454-4-5
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