Encephalitogenic Activity of Poly-L-lysine

Kornguth, Steven; Bennett, D. R.; Thompson, Hartwell G.; ZuRhein, Gabriele M.; Stahmann, Mark A.

doi:10.1038/1931081a0

Cited by 2 publications

(1 citation statement)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One mg of polylysine in itself produced no morphological alteration of a normal healthy myelinated culture. Thus, in ~tro there appears to be no affinity of the demyelinating factor for a non-specific basic protein, nor does the protein initiate or facilitate demyelination in vitro as it has been demonstrated to do in vivo (5).…”

Section: Resultsmentioning

confidence: 98%

The Application of Tissue Culture to the Study of Experimental Allergic Encephalomyelitis

Appel

Bornstein

1964

The Journal of Experimental Medicine

133

View full text Add to dashboard Cite

Myelinated cultures of rat and mouse cerebellum undergo a specific and characteristic pattern of demyelination in the presence of sera from animals with experimental allergic encephalomyelitis (EAE) (1, 2). The neuroglia swell; myelin sheaths become disfigured b y fusiform swellings and break away as small fragments; and finally, remaining intact sheaths and myelin fragments are reduced to small fat droplets. During this process neuron somas and axons appear little affected (Figs. 1 to 4).This communication will present evidence for an immunological mechanism responsible for the in vitro demyelination. MethodsThe techniques of rat cerebellar tissue culture, induction of EAE in animals, and the preparation of sera have been previously described (1). An additional technique was employed to develop a series of animals with varying incidence of clinical and pathological lesions and varying levels of circulating antibodies. Each of 10 rabbits received 3 intraperitoneal inoculations of bovine cord (250 mg each) over a 3 month period: 5 animals with cord suspension in Freund's adjuvant; and the remaining 5, with cord in saline. Four of the 5 animals inoculated with cord in adjuvant developed hindleg weakness following the third inoculation, which progressed over 2 to 4 weeks to complete paraplegia, urinary and fecal incontinence, and death. At autopsy, 4 months after the first inoculation, characteristic lesions of EAE were found. Two of the remaining animals, i.e. without adjuvant, developed hindleg weakness and ataxia following the third inoculation. However, at autopsy, 4 months after the first inoculation and 2 weeks after serum examination and the appearance of symptoms, no microscopic nervous system changes were noted.

show abstract

Section: Resultsmentioning

confidence: 98%