Myelination Inhibiting and Neuroelectric Blocking Factors in Experimental Allergic Encephalomyelitis

Seil, Fredrick J.; Smith, M.G.H.; Leiman, Arnold L.; Kelly, James M.

doi:10.1126/science.49925

Cited by 44 publications

(17 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is in marked contrast with recent tissue culture studies (Seil et al, 1975) in which blocking activity was equally abundant in a variety of control sera. A possible explanation of these studies is that the electrical activity found in tissue culture systems is relatively more labile and sensitive to a component of normal serum which the frog spinal cord is either insensitive to, or which is masked by the VRR potentiating effect characteristic of normal serum.…”

Section: Discussioncontrasting

confidence: 96%

“…increase in VRR. In no case was the VRR significantly decreased by normal serum, in contrast with the results obtained on cultured CNS tissue (Seil et al, 1975(Seil et al, , 1976. 682 Our data on the potentiation by control sera agree fairly well with that of Cerf and Carels (1966) who obtained an average 42% increase (range 9%/O to 84%) in VRR in 12 preparations.…”

Section: Resultssupporting

confidence: 81%

“…In contrast with these results, Seil et al (1975Seil et al ( , 1976 reported in extensive studies that the neuroelectric blocking factor(s) claimed by Bornstein and Crain (1965) to exist specifically in EAE and MS sera were also present to a comparable extent in a variety of control sera. Using mouse cerebral neocortex cultures, they found no significant difference between the blocking activity of sera from MS patients and normal subjects, or between the sera of rats injected with guinea-pig white matter in Freund's complete adjuvant (FCA) and those injected with various control antigens, including FCA alone.…”

contrasting

confidence: 63%

See 2 more Smart Citations

Neuroelectric blocking factors in human and animal sera evaluated using the isolated frog spinal cord.

Schauf¹,

Davis²,

Sack³

et al. 1976

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

s The effects of sera from guinea-pigs with experimental allergic encephalomyelitis (EAE) and multiple sclerosis (MS) patients were evaluated and compared with the activity of control sera using the isolated frog spinal cord. Ventral root responses (VRR) were recorded during supramaximal ipsilateral dorsal root stimulation in the presence and absence of 25% serum. In control experiments with normal human and guinea-pig sera we observed a consistent, reversible increase in VRR averaging 20% and 17% respectively, and in no case was any significant decrease produced. In contrast, sera from EAE guinea-pigs 12 to 19 days after injection produced an equally rapid, reversible decrease in VRR. The decrease averaged 36% and was highly significant (P<0.0001) relative to controls. Similarly, sera from MS patients on the average decreased the VRR by 26%, and this again was significant compared with controls (P<10-6).

show abstract

Section: Discussioncontrasting

confidence: 96%

Section: Resultssupporting

confidence: 81%

contrasting

confidence: 63%

See 1 more Smart Citation

Neuroelectric blocking factors in human and animal sera evaluated using the isolated frog spinal cord.

Schauf¹,

Davis²,

Sack³

et al. 1976

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

show abstract

“…The suspicion that such factors may exist originated with a study showing that sera from animals with experimental autoimmune encephalomyelitis or from MS patients during acute exacerbation, blocked re£ex activity in cultured central nervous system (CNS) tissue within minutes of exposure and in a complement-dependent manner (Bornstein & Crain 1965). The study was quite small and included few controls, but it was followed by a series of studies which reached similar conclusions (Cerf & Carels 1966;Carels & Cerf 1969;Lumsden et al 1975a,b;Schauf et al 1976 and some others which threw doubt on the interpretation of the data (Crain et al 1975;Seil et al 1975Seil et al , 1976, claiming that the blocking activity was not speci¢c to MS. Where present, the conduction block appears to be contained within the IgG-containing fraction of serum (Crain et al 1975; and it is diminished by plasma exchange Stefoski et al 1982). However, if antibodies are involved, they probably act by means other than demyelination, since the blocking activity is both prompt and reversible.…”

Section: (Iv) Neuroelectric Blocking Factorsmentioning

confidence: 95%

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

Smith

McDonald

1999

Phil. Trans. R. Soc. Lond. B

290

181

View full text Add to dashboard Cite

The pathophysiology of multiple sclerosis is reviewed, with emphasis on the axonal conduction properties underlying the production of symptoms, and the course of the disease. The major cause of the negative symptoms during relapses (e.g. paralysis, blindness and numbness) is conduction block, caused largely by demyelination and inflammation, and possibly by defects in synaptic transmission and putative circulating blocking factors. Recovery from symptoms during remissions is due mainly to the restoration of axonal function, either by remyelination, the resolution of inflammation, or the restoration of conduction to axons which persist in the demyelinated state. Conduction in the latter axons shows a number of deficits, particularly with regard to the conduction of trains of impulses and these contribute to weakness and sensory problems. The mechanisms underlying the sensitivity of symptoms to changes in body temperature (Uhthoff's phenomenon) are discussed. The origin of ‘positive’ symptoms, such as tingling sensations, are described, including the generation of ectopic trains and bursts of impulses, ephaptic interactions between axons and/or neurons, the triggering of additional, spurious impulses by the transmission of normal impulses, the mechanosensitivity of axons underlying movement–induced sensations (e.g. Lhermitte's phenomenon) and pain. The clinical course of the disease is discussed, together with its relationship to the evolution of lesions as revealed by magnetic resonance imaging and spectroscopy. The earliest detectable event in the development of most new lesions is a breakdown of the blood–brain barrier in association with inflammation. Inflammation resolves after approximately one month, at which time there is an improvement in the symptoms. Demyelination occurs during the inflammatory phase of the lesion. An important mechanism determining persistent neurological deficit is axonal degeneration, although persistent conduction block arising from the failure of repair mechanisms probably also contributes.

show abstract

“…Kies et a1 [48] similarly demonstrated that most sera from myelin basic protein-sensitized guinea pigs with high titers of anti-basic protein antibody fail to prevent myelination upon application to cerebellar cultures from the time of explanation. This demonstration was repeated with sera from subhuman primates [73], rabbits [7 11, and Lewis rats [74] [37,42] might be due to contamination with minute amounts of other myelin fractions. The possibility remains that cerebroside induction of serum antimyelin factors is a phenomenon peculiar to rabbits, and studies are under way to examine this question.…”

Section: Eae and Serum Antimyelin Activitymentioning

confidence: 91%

Tissue culture studies of demyelinating disease: A critical review

Seil

1977

Annals of Neurology

Self Cite

View full text Add to dashboard Cite

Tissue culture studies of human and experimental demyelinating diseases have demonstrated that sera from patients with multiple sclerosis reversibly demyelinate central nervous system cultures. Similar changes are evoked by sera from animals with experimental allergic encephalomyelitis induced by inoculation with whole central nervous system tissue but not by encephalitogenic myelin basic protein. Sera and buffy coat or lymph node cells from humans with idiopathic polyneuritis and animals with experimental allergic neuritis demyelinate cultures of peripheral nervous system tissue. While these studies have contributed to speculations about pathogenetic mechanisms of demyelinating diseases, including the role of both circulating antibodies and delayed hypersensitivity factors, a number of important questions remain unanswered. Among these are the identity of the antigens that evoke antimyelin antibodies and the precise relationship of serum or cellular antimyelin factors to the pathogenesis or clinical course of the demyelinating diseases. Further studies with this technique may provide more complete information about the role of immunological events in induction of disease.

show abstract

Myelination Inhibiting and Neuroelectric Blocking Factors in Experimental Allergic Encephalomyelitis

Cited by 44 publications

References 17 publications

Neuroelectric blocking factors in human and animal sera evaluated using the isolated frog spinal cord.

Neuroelectric blocking factors in human and animal sera evaluated using the isolated frog spinal cord.

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

Tissue culture studies of demyelinating disease: A critical review

Contact Info

Product

Resources

About