Saltatory conduction precedes remyelination in axons demyelinated with lysophosphatidyl choline☆
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Multiple Sclerosis: Mechanisms of Disease and Strategies for Myelin and Axonal Repair
2018, Neurologic ClinicsCitation Excerpt :After an acute injury in peripheral axons, there is a high density of sodium channels.68 Murine models of demyelination have also shown how formation of nodes of Ranvier (where action potentials are generated) and saltatory conduction precedes remyelination in axons with demyelination.69 Demyelinated mice with MHC class I deficiency and normal functional status have been previously described.55
Demyelination in multiple sclerosis
2014, Handbook of Clinical NeurologyCitation Excerpt :These changes, which take 2–3 weeks to develop, may facilitate the restoration of conduction across the demyelinated segment (Smith et al., 1981). However, in this circumstance, conduction along demyelinated axons is no longer saltatory and fast but, rather, is continuous and slow (Smith et al., 1982). In other circumstances, conduction block may persist and such an outcome is favored by factors such as a large axon diameter (Bostock and Sears, 1978), a long length of demyelination, the absence of any glial ensheathment (Shrager and Rubinstein, 1990), and the presence of deleterious factors such as nitric oxide (Redford et al., 1997).
Rolipram promotes remyelination possibly via MEK-ERK signal pathway in cuprizone-induced demyelination mouse
2012, Experimental NeurologyCitation Excerpt :Increased cAMP has been reported to overcome myelin-associated inhibitors to promote axonal regeneration (Domeniconi and Filbin, 2005). Lysolecithin (LPC) induces demyelination because it has high affinity to myelin basic protein (MBP) (Smith et al., 1982). Cuprizone‐induceddemyelination is results from the degeneration of supporting oligodendrocytes rather than from a direct impact on myelin sheaths (Kipp et al., 2009).
Experimental in vivo and in vitro models of multiple sclerosis: EAE and beyond
2012, Multiple Sclerosis and Related DisordersCitation Excerpt :The most commonly used toxins for focal demyelination are EB and LPC. Both agents have been used to induce demyelination in certain brain areas such as the striatum (Degaonkar et al., 2002), hippocampal formation (Goudarzvand et al., 2010), spinal cord tissue (Ousman and David, 2000; Triarhou and Herndon, 1986), optic nerve (Carroll et al., 1983), ventral roots (Smith et al., 1982), caudal cerebellar peduncles (Penderis et al., 2003) or corpus callosum (Jablonska et al., 2010). Demyelination can also be induced in the peripheral nervous system (Hall, 1973).
NG2-glia as Multipotent Neural Stem Cells: Fact or Fantasy?
2011, NeuronCitation Excerpt :Perhaps de novo myelination and myelin replacement go on concurrently in different parts of the CNS or within axon tracts, such as the corpus callosum, that contain a mixture of myelinated and unmyelinated axons. If myelin turnover turns out to be commonplace, how neural pathways can cope with continual loss and replacement of oligodendrocytes would need to be understood, because the loss of even one myelin internode has been predicted to cause conduction block (Koles and Rasminsky, 1972; Waxman and Brill, 1978; Smith et al., 1982). Whether action potentials are blocked or delayed will depend on the geometry of the affected fibers, including internode length and axon diameter (e.g., Bostock and Sears, 1976; Waxman and Brill, 1978; Bakiri et al., 2010).
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This work was supported by a grant from the Medical Research Council of Great Britain.