Axonal signals in central nervous system myelination, demyelination and remyelination

Coman, Irène; Barbin, G.; Charles, Perrine; Zalc, Bernard; Lubetzki, Catherine

doi:10.1016/j.jns.2005.03.029

Cited by 81 publications

(53 citation statements)

References 32 publications

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“…In cultured embryonic rat motor neurons, knockdown of multiple sodium channel α-subunit isoforms caused by transfection of small hairpin RNAs decreased expression of functional sodium channels at the axon initial segment, thereby interfering with heteroprotein complex formation between ankyrin G , neuronal cell adhesion molecule, and neurofascin at the axon initial segment. Previous studies have shown that neuronal cell adhesion molecule and L1 cell adhesion molecule regulated axon myelination and remyelination, which were summarized in a review article (13).…”

Section: Central Nervous Systemmentioning

confidence: 99%

“…However, little is known about the mechanisms governing the onset of axon myelination by electrical activity (13,32). Electrical activity-dependent communication between axons and myelinating glial cells can occur in the vicinity of axolemma away from the synapse (7).…”

Section: Central Nervous Systemmentioning

confidence: 99%

“…In multiple sclerosis, loss of myelin sheath and loss of axon occur within the white matter of the brain and spinal cord (13,32,44). In mice being rendered to experimental autoimmune encephalomyelitis, an animal model of human multiple sclerosis, Na v 1.2 and Na v 1.6 distributed diffusely along almost the entire length of demyelinated axons of the optic nerve, with the upregulation of Na v 1.2 mRNA level (44, 49 -51).…”

Section: Sodium Channel Remodeling In Neurodegeneration: Demyelinatiomentioning

confidence: 99%

“…In addition to multiple sclerosis, demyelination can be induced in various diseases (e.g., viral infection and spinal cord injury) (13,32,33,44). Autopsy studies in humans and animals have increasingly pointed out that demyelination is necessary, but not sufficient per se for development of permanent deficits in multiple sclerosis; substantial demyelination can be observed in apparently normal individuals with no neurological deficits during their life (45,98,99).…”

Section: Sodium Channel Remodeling In Neurodegeneration: Demyelinatiomentioning

confidence: 99%

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Roles of Voltage-Dependent Sodium Channels in Neuronal Development, Pain, and Neurodegeneration

Wada

2006

J Pharmacol Sci

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Abstract. Besides initiating and propagating action potentials in established neuronal circuits, voltage-dependent sodium channels sculpt and bolster the functional neuronal network from early in embryonic development through adulthood (e.g., differentiation of oligodendrocyte precursor cells into oligodendrocytes, myelinating axon; competition between neighboring equipotential neurites for development into a single axon; enhancing and opposing functional interactions with attractive and repulsive molecules for axon pathfinding; extending and retracting terminal arborization of axon for correct synapse formation; experience-driven cognition; neuronal survival; and remyelination of demyelinated axons). Surprisingly, different patterns of action potentials direct homeostasis-based epigenetic selection for neurotransmitter phenotype, thus excitability by sodium channels specifying expression of inhibitory neurotransmitters. Mechanisms for these pleiotropic effects of sodium channels include reciprocal interactions between neurons and glia via neurotransmitters, growth factors, and cytokines at synapses and axons. Sodium channelopathies causing pain (e.g., allodynia) and neurodegeneration (e.g., multiple sclerosis) derive from 1) electrophysiological disturbances by insults (e.g., ischemia / hypoxia, toxins, and antibodies); 2) loss-of-physiological function or gain-of-pathological function of mutant sodium channel proteins; 3) spatiotemporal inappropriate expression of normal sodium channel proteins; or 4) de-repressed expression of otherwise silent sodium channel genes. Na v 1.7 proved to account for pain in human erythermalgia and inflammation, being the convincing molecular target of pain treatment.

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Section: Central Nervous Systemmentioning

confidence: 99%

Section: Central Nervous Systemmentioning

confidence: 99%

Section: Sodium Channel Remodeling In Neurodegeneration: Demyelinatiomentioning

confidence: 99%

Section: Sodium Channel Remodeling In Neurodegeneration: Demyelinatiomentioning

confidence: 99%

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Roles of Voltage-Dependent Sodium Channels in Neuronal Development, Pain, and Neurodegeneration

Wada

2006

J Pharmacol Sci

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“…PSA down regulation in OPC seems to be critical for proper maturation of OPC into myelinating mature oligodendrocytes (Charles et al, 2000(Charles et al, , 2002Koutsoudaki et al, 2010). Polysialylation of NCAM appears to be regulated at the posttranslational level since overexpression of polysialyltransferases by ectopic expression is not sufficient to maintain PSA expression and only delays myelination (Coman et al, 2005). These experiments however did not elucidate whether this occurs in a cell-autonomous manner or following interactions with axons to be remyelinated.…”

Section: Polysialylation Results In Plasticity At the Cellular Scalementioning

confidence: 98%

Polysialylation of the Neural Cell Adhesion Molecule: Setting the Stage for Plasticity Across Scales of Biological Organization

Amoureux¹,

Viallat²,

Giribone³

et al. 2012

Chemical Biology

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Axonal Regeneration and Myelination: Applicabilityof the Layer‐by‐Layer Technology

Pyne

Baek

et al. 2015

Layer‐by‐Layer Films for Biomedical Applications

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Axonal signals in central nervous system myelination, demyelination and remyelination

Cited by 81 publications

References 32 publications

Roles of Voltage-Dependent Sodium Channels in Neuronal Development, Pain, and Neurodegeneration

Roles of Voltage-Dependent Sodium Channels in Neuronal Development, Pain, and Neurodegeneration

Polysialylation of the Neural Cell Adhesion Molecule: Setting the Stage for Plasticity Across Scales of Biological Organization

Axonal Regeneration and Myelination: Applicabilityof the Layer‐by‐Layer Technology

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