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C E Lumsden

Publications and source records attributed to C E Lumsden.

18 recordsLinked to original sources
PubMed1975

Anti-synaptic antibody in allergic encephalomyelitis. I. Neurophysiological studies, in guinea pigs, on the exposed cerebral cortex and peripheral nerves, following immunological challenges with myelin and synaptosomes.

The potential evoked at the surface of the cerebral cortex of a guinea pig, by stimulation of the contralateral forepaw, usually consists of an initial double positive wave whose waveform remains unchanged during rapid stimulation. In a guinea pig with experimental allergic encephalomyelitis (EAE) the response is attenuated at low frequencies of stimulation. Observations were also made on animals with experimental allergic neuritis (AEN). These animals showed a peripheral specificity for decreased conduction velocity, but have normal cortical evoked responses. Histological studies were undertaken in parallel with the electrophysiological studies and the concordance and discordance between the two is discussed. We conclude that there is no evident correlation between the severity of the electrophysiological effects and the histological lesions. An attempt was also made to induce an immunological challenge in guinea pigs, in the same way that EAE and EAN is produced, by the injection of synaptosomes. No clinical signs or alterations in the histology or electrophysiology of the animals were seen. A discussion is included on the elucidation of the site of action of EAE by discriminating between the direct effects on myelin and synapses and by the indirect effects of myelin damage on synapses. No firm conclusion is reached and the matter is left for further analysis in the subsequent paper. Finally, the neurophysiological alterations, demonstrated in the EAE and EAN situations, are discussed in terms of a humoral factor possibly acting on the myelin sheath and indirectly affecting synaptic function. This matter is further discussed in the subsequent paper.

Animals↗
PubMed1975

Anti-synaptic antibody in allergic encephalomyelitis. II. The synapse-blocking effects in tissue culture of demyelinating sera from experimental allergic encephalomyelitis.

It has been suggested that demyelination cannot account for all of the observed clinical symptoms of multiple sclerosis (MS), in particular the rapidity of onset and remission of the disease, and attention has been focussed on the role of the synapse in 'demyelinating diseases'. In the present paper we have attempted to resolve the fundamental question of the site of action of a demyelinating disease, experimental allergic encephalomyelitis (EAE), by the use of cultures of neonatal rat cerebellum. Electrophysiological and morphological development in these cultures run hand-in-hand, and in the first few days in vitro there is a 4-5 day period when synapses are both seen ultrastructurally and known to be functioning but before the onset of myelination. The serum from guinea pigs with EAE was added to these cultures at different stages during their development and the morphological and electrophysiological effects observed. An abolitionary effect on the bioelectric activity of the culture was only observed when the serum was added to mature, myelinated cultures. Also the same active sera had no effect on synaptic activity before myelination had occurred. We conclude that the synaptic blocking effect occurs only when myelin is destroyed.

Animals↗
PubMed1975

Binding of normal human IgG to myelin sheaths, glia and neurons.

The binding of normal human serum, purified IgG and IgG fragments to central nervous tissue was studied by the anti-globulin consumption (AGCT) and immunofluorescence (IF) techniques. In the AGCT, F(ab')2 fragments failed to react, whereas IgG and Fc fragments did so. In IF experiments, the binding was localized to myelin sheaths, glia and neurons; Fab monomers at a protein concentration of 1-3 mg/ml dod not react with the tissue, but purified Fc fragments at 0-0625 mg/ml did. The binding is neither tissue- nor species-specific. Lipid and protein extraction procedures indicated that the factor responsible for binding to myelin was basic protein. It was concluded that the binding of normal IgG to central nervous tissue is medicated by the Fc part of the molecule.

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