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Nucleic Acid and Protein Metabolism in White MatterObservations During Experimental Demyelination and Remyelination; a Histochemical and Autoradiographic Study of Spinal Cord of the Adult Cat
HAROLD KOENIG, M.D.;
MARY BARTLETT BUNGE, Ph.D.;
RICHARD P. BUNGE, M.D.
Arch Neurol. 1962;6(3):177-193.
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Introduction
The experimental lesion produced by cerebrospinal fluid exchange provides an unusual opportunity to investigate demyelination and remyelination in the adult mammalian neuraxis. The lesion was discovered empirically when animals subjected to repeated withdrawal and reinjection of cerebrospinal fluid (CSF) were observed to develop conspicuous neurological deficits.1 Though the mechanism by which this lesion is produced remains unknown, the unique occurrence of remyelination following demyelination has provided impetus for light and electron microscopic studies1-3 and for this autoradiographic analysis. Taken together, these studies indicate that adult glial cells have a degree of versatility not hitherto recognized.
To produce the lesion nothing is added to the CSF; it is simply withdrawn and reinjected repeatedly through a needle in the cisterna magna. A portion of animals so treated ( 40%) develop partial paralysis of the posterior extremities; the more severely affected are unable to walk. At autopsy the lesion is
. . . [Full Text PDF of this Article]
Author Affiliations
CHICAGO; NEW YORK
From the Neurology and the Radioisotope Services, Veterans Administration Research Hospital, and the Department of Neurology and Psychiatry, Northwestern University Medical School, Chicago (Dr. Koenig), and the Department of Anatomy, the Medical School, and the Department of Zoology, University of Wisconsin, Madison (Dr. R. P. Bunge and Dr. M. B. Bunge).
Postdoctoral Fellow of the National Institute of Neurological Diseases and Blindness (Dr. M. B. Bunge); Postdoctoral Fellow of the National Multiple Sclerosis Society (Dr. R. P. Bunge). The Doctors Bunge are presently in the Department of Anatomy and the Laboratory for Cell Physiology, Columbia University College of Physicians and Surgeons.
Footnotes
Received for publication Oct. 3, 1961.
With the technical assistance of Barbara Rich and Dorothy Thomas.
A portion of this paper was presented before the American Association of Neuropathology, Boston, June, 1960.
This study was supported by Grant B-1456(C1) and (C2) from the National Institutes of Health of the U.S. Public Health Service, and Contract No. AT (11-1)-89 from the U.S. Atomic Energy Commission to Dr. Koenig, and by Grant B-1661 from the National Institutes of Health of the U.S. Public Health Service, the Research Committee of the University of Wisconsin, from funds contributed by the Wisconsin Alumni Research Foundation and the Medical School Research Committee and Department of Neurology at the University of Wisconsin to Dr. R. P. Bunge and Dr. M. B. Bunge.
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