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STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM

Rolling disease has been produced and studied in rats and mice, using the exotoxin of the A strain of Mycoplasma neurolyticum. The primary lesion of the brain consists of spongiform degeneration, associated with vesicle formation in the cortex and underlying white matter of the cerebral hemispheres,...

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Detalles Bibliográficos
Autores principales: Thomas, Lewis, Aleu, Fernando, Bitensky, Mark W., Davidson, Morton, Gesner, Bertram
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1966
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2138330/
https://www.ncbi.nlm.nih.gov/pubmed/5925313
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author Thomas, Lewis
Aleu, Fernando
Bitensky, Mark W.
Davidson, Morton
Gesner, Bertram
author_facet Thomas, Lewis
Aleu, Fernando
Bitensky, Mark W.
Davidson, Morton
Gesner, Bertram
author_sort Thomas, Lewis
collection PubMed
description Rolling disease has been produced and studied in rats and mice, using the exotoxin of the A strain of Mycoplasma neurolyticum. The primary lesion of the brain consists of spongiform degeneration, associated with vesicle formation in the cortex and underlying white matter of the cerebral hemispheres, and in the molecular layer of the cerebellum. The brains of animals surviving 2 days or longer show extensive necrotizing lesions resembling ischemic necrosis, in both cerebral hemispheres. The brains of rats and mice with rolling disease become deeply stained by intraperitoneally injected trypan blue, indicating early disruption of the blood brain barrier. The toxin appears to be a thermolabile protein with a molecular weight exceeding 200,000. It is only active when injected by vein, and causes no disease when injected intracerebrally, intraperitoneally or subcutaneously, suggesting the existence of specific receptors within the vascular bed of the central nervous system. Protection is afforded by rabbit antibody against the toxin, but only when antibody is injected within less than 3 min after intravenous injection of toxin, indicating rapid fixation to receptors in the brain. The toxin is inactivated by incubation for 10 min at 37°C with suspensions of the sedimentable component of normal brain. The inactivating factor in brain sediment is very thermostable, not affected by trypsin, and eliminated by treatment with periodate. Similar inactivation of toxin is demonstrable with water-soluble gangliosides of brain. A theoretical concept to explain the action of the toxin is proposed.
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spelling pubmed-21383302008-04-17 STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM Thomas, Lewis Aleu, Fernando Bitensky, Mark W. Davidson, Morton Gesner, Bertram J Exp Med Article Rolling disease has been produced and studied in rats and mice, using the exotoxin of the A strain of Mycoplasma neurolyticum. The primary lesion of the brain consists of spongiform degeneration, associated with vesicle formation in the cortex and underlying white matter of the cerebral hemispheres, and in the molecular layer of the cerebellum. The brains of animals surviving 2 days or longer show extensive necrotizing lesions resembling ischemic necrosis, in both cerebral hemispheres. The brains of rats and mice with rolling disease become deeply stained by intraperitoneally injected trypan blue, indicating early disruption of the blood brain barrier. The toxin appears to be a thermolabile protein with a molecular weight exceeding 200,000. It is only active when injected by vein, and causes no disease when injected intracerebrally, intraperitoneally or subcutaneously, suggesting the existence of specific receptors within the vascular bed of the central nervous system. Protection is afforded by rabbit antibody against the toxin, but only when antibody is injected within less than 3 min after intravenous injection of toxin, indicating rapid fixation to receptors in the brain. The toxin is inactivated by incubation for 10 min at 37°C with suspensions of the sedimentable component of normal brain. The inactivating factor in brain sediment is very thermostable, not affected by trypsin, and eliminated by treatment with periodate. Similar inactivation of toxin is demonstrable with water-soluble gangliosides of brain. A theoretical concept to explain the action of the toxin is proposed. The Rockefeller University Press 1966-11-30 /pmc/articles/PMC2138330/ /pubmed/5925313 Text en Copyright © 1966 by The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Thomas, Lewis
Aleu, Fernando
Bitensky, Mark W.
Davidson, Morton
Gesner, Bertram
STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title_full STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title_fullStr STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title_full_unstemmed STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title_short STUDIES OF PPLO INFECTION : II. THE NEUROTOXIN OF MYCOPLASMA NEUROLYTICUM
title_sort studies of pplo infection : ii. the neurotoxin of mycoplasma neurolyticum
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2138330/
https://www.ncbi.nlm.nih.gov/pubmed/5925313
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