Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats
(1988) In Acta Neuropathologica 76(5). p.441-450- Abstract
- The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of... (More)
- The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1104228
- author
- Fredriksson, K ; Kalimo, H ; Nordborg, C ; Olsson, Y and Johansson, Barbro LU
- organization
- publishing date
- 1988
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Stroke-prone spontaneously hypertensive rats, Blood-brain barrier, Brain oedema, Astrocytes, Glial fibrillary acidic protein
- in
- Acta Neuropathologica
- volume
- 76
- issue
- 5
- pages
- 441 - 450
- publisher
- Springer
- external identifiers
-
- pmid:3188837
- scopus:0023686958
- ISSN
- 1432-0533
- DOI
- 10.1007/BF00686382
- language
- English
- LU publication?
- yes
- id
- dacb3ffe-0901-4221-835a-945f0ee73b83 (old id 1104228)
- date added to LUP
- 2016-04-01 17:01:03
- date last changed
- 2021-01-03 10:37:28
@article{dacb3ffe-0901-4221-835a-945f0ee73b83,
abstract = {{The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma.}},
author = {{Fredriksson, K and Kalimo, H and Nordborg, C and Olsson, Y and Johansson, Barbro}},
issn = {{1432-0533}},
keywords = {{Stroke-prone spontaneously hypertensive rats; Blood-brain barrier; Brain oedema; Astrocytes; Glial fibrillary acidic protein}},
language = {{eng}},
number = {{5}},
pages = {{441--450}},
publisher = {{Springer}},
series = {{Acta Neuropathologica}},
title = {{Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats}},
url = {{http://dx.doi.org/10.1007/BF00686382}},
doi = {{10.1007/BF00686382}},
volume = {{76}},
year = {{1988}},
}