Ephaptic transmission between single nerve fibres in the spinal nerve roots of dystrophic mice.

Rasminsky, Michael

doi:10.1113/jphysiol.1980.sp013356

Cited by 165 publications

(62 citation statements)

References 30 publications

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“…This condition is fulfilled, for instance, in bundles of unmyelinated axons where the periaxonal space is minimal, as in olfactory nerves (62,68). Ephaptic interactions between axons have also been observed in frog sciatic nerve (288) and in demyelinated spinal axons of dystrophic mice (436).…”

Section: Ephaptic Interactions and Axonal Spike Synchronizationmentioning

confidence: 95%

Axon Physiology

Debanne

Campanac

Bialowas

et al. 2011

Physiological Reviews

557

492

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Axons are generally considered as reliable transmission cables in which stable propagation occurs once an action potential is generated. Axon dysfunction occupies a central position in many inherited and acquired neurological disorders that affect both peripheral and central neurons. Recent findings suggest that the functional and computational repertoire of the axon is much richer than traditionally thought. Beyond classical axonal propagation, intrinsic voltage-gated ionic currents together with the geometrical properties of the axon determine several complex operations that not only control signal processing in brain circuits but also neuronal timing and synaptic efficacy. Recent evidence for the implication of these forms of axonal computation in the short-term dynamics of neuronal communication is discussed. Finally, we review how neuronal activity regulates both axon morphology and axonal function on a long-term time scale during development and adulthood.

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Section: Ephaptic Interactions and Axonal Spike Synchronizationmentioning

confidence: 95%

Axon Physiology

Debanne

Campanac

Bialowas

et al. 2011

Physiological Reviews

557

492

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“…The clinical observations suggest that warming will promote conduction block, with the opposite e¡ect upon cooling, and these consequences have often been demonstrated in peripheral demyelinated axons (Davis & Jacobson 1971;Rasminsky 1973;Davis et al 1975;Pencek et al 1980;Pender & Sears 1984). While examining central demyelinated axons, one of the authors (K.J.S.)…”

Section: E¡ects Of Temperaturementioning

confidence: 99%

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

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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.

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“…There have been multiple demonstrations of ephaptic interactions that can lead to ectopic impulse activity, not only between closely apposed uninjured axons (56) but also between injured axons (57,58) and between neighboring dysmyelinated axons (59). It has been suggested that demyelination due to compression is present in some cases of trigeminal neuralgia (2,60,61).…”

Section: Acknowledgmentsmentioning

confidence: 99%