The Glial response to injury in the developing brain
The Glial response to injury in the developing brain
Despite major advances in techniques of imaging the human brain, there is still uncertainty about the exact time at which many fetal and neonatal brain lesions occur. Pathological appearances do not always help owing to the difficulty in establishing the exact sequence of the tissue response to brain injury. In the first part of the present study, 179 post-mortem human brains from fetal, neonatal and infant cases (varying in age from the first trimester of gestation to children of 7 years of age) were examined macroscopically and by light microscopy. Of these brains, 69 showed no pathological abnormality, 98 had hypoxic/ischaemic lesions, 5 displayed congenital abnormalities and 4 brains showed venous infarcts. Hypoxic/ischaemic brain damage was the most common lesion in this series and affected fetuses from 16 weeks of gestation to term and infants who had survived to 19 months of age. This group was ideal for studying the glial, inflammatory and blood vessel responses to brain damage in fetal and early postnatal life. Light microscopical studies included immunocytochemistry for Glial Fibrillary Acidic Protein (GFAP) - an astrocyte marker, S-100 protein - a glial marker, fibronectin - a marker for the connective tissue in blood vessel walls, factor VIII Related Antigen - an endothelial cell marker and S22 - a macrophage marker. The expression of these markers was also assessed in the normal developing human brain. The second part of the study was designed to test the hypothesis that GFAP could be induced by injury to the fetal brain before the time at which it appears during normal fetal development. Cold lesions were inflicted upon fetal and neonatal rat brains and the glial response was examined by the immunoperoxidase staining technique. The expression of glial and mesenchymal cell markers in developing uninjured fetal and neonatal animals was also assessed. The results of this combined human and experimental study suggest that: a) The expression of GFAP by developing astrocytes can be induced by injury to the CNS in an area and at a time at which it is not observed in the normal developing brain b) In the human brain, formation of glial scar tissue occurs as early as 22 weeks of gestation in fetuses with hypoxic/ischaemic brain damage c) After 22 weeks gestation in man and 16 day gestation in the rat, the formation of glial scar tissue depends on the period elapsing from the time of injury to the moment of death, irrespective of age. d) The glial response is similar in different types of injury and in brains injured in utero or in postnatal life. Following this study a more logical approach has been adopted for the assessment of fetal and neonatal brain damage. (DX86661)
University of Southampton
Moore, Isabella Elizabeth
1988
Moore, Isabella Elizabeth
Moore, Isabella Elizabeth
(1988)
The Glial response to injury in the developing brain.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Despite major advances in techniques of imaging the human brain, there is still uncertainty about the exact time at which many fetal and neonatal brain lesions occur. Pathological appearances do not always help owing to the difficulty in establishing the exact sequence of the tissue response to brain injury. In the first part of the present study, 179 post-mortem human brains from fetal, neonatal and infant cases (varying in age from the first trimester of gestation to children of 7 years of age) were examined macroscopically and by light microscopy. Of these brains, 69 showed no pathological abnormality, 98 had hypoxic/ischaemic lesions, 5 displayed congenital abnormalities and 4 brains showed venous infarcts. Hypoxic/ischaemic brain damage was the most common lesion in this series and affected fetuses from 16 weeks of gestation to term and infants who had survived to 19 months of age. This group was ideal for studying the glial, inflammatory and blood vessel responses to brain damage in fetal and early postnatal life. Light microscopical studies included immunocytochemistry for Glial Fibrillary Acidic Protein (GFAP) - an astrocyte marker, S-100 protein - a glial marker, fibronectin - a marker for the connective tissue in blood vessel walls, factor VIII Related Antigen - an endothelial cell marker and S22 - a macrophage marker. The expression of these markers was also assessed in the normal developing human brain. The second part of the study was designed to test the hypothesis that GFAP could be induced by injury to the fetal brain before the time at which it appears during normal fetal development. Cold lesions were inflicted upon fetal and neonatal rat brains and the glial response was examined by the immunoperoxidase staining technique. The expression of glial and mesenchymal cell markers in developing uninjured fetal and neonatal animals was also assessed. The results of this combined human and experimental study suggest that: a) The expression of GFAP by developing astrocytes can be induced by injury to the CNS in an area and at a time at which it is not observed in the normal developing brain b) In the human brain, formation of glial scar tissue occurs as early as 22 weeks of gestation in fetuses with hypoxic/ischaemic brain damage c) After 22 weeks gestation in man and 16 day gestation in the rat, the formation of glial scar tissue depends on the period elapsing from the time of injury to the moment of death, irrespective of age. d) The glial response is similar in different types of injury and in brains injured in utero or in postnatal life. Following this study a more logical approach has been adopted for the assessment of fetal and neonatal brain damage. (DX86661)
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Published date: 1988
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Local EPrints ID: 461096
URI: http://eprints.soton.ac.uk/id/eprint/461096
PURE UUID: 3a8628f1-83f2-48ab-8b55-3cb43d24816b
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Date deposited: 04 Jul 2022 18:35
Last modified: 04 Jul 2022 18:35
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Author:
Isabella Elizabeth Moore
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