Saltatory conduction in single isolated and non‐isolated myelinated nerve fibres

Bishop, Peter; Levick, W. R.

doi:10.1002/jcp.1030480102

Cited by 10 publications

(5 citation statements)

References 15 publications

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“…Early investigations of AP propagation in myelinated axons indicated propagation occurs in a "saltatory" manner, progressing along the axon by jumping between active nodes of Ranvier (Huxley and Stampfli, 1949;Bishop and Levick, 1956). As indi- Figure 5.…”

Section: Development Of Action Potential Initiation and Propagationmentioning

confidence: 99%

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

2006

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Fundamental to an understanding of how neurons integrate synaptic input is the knowledge of where within a neuron this information is converted into an output signal, the action potential. Although it has been known for some time that action potential initiation occurs within the axon of neurons, the precise location has remained elusive. Here, we provide direct evidence using voltage-sensitive dyes that the site of action potential initiation in cortical layer 5 pyramidal neurons is ϳ35 m from the axon hillock. This was the case during action potential generation under a variety of conditions, after axonal inhibition, and at different stages of development. Once initiated action potentials propagated down the axon in a saltatory manner. Experiments using local application of low-sodium solution and TTX, as well as an investigation of the influence of axonal length on action potential properties, provided evidence that the initial 40 m of the axon is essential for action potential generation. To morphologically identify the relationship between the site of action potential initiation and axonal myelination, we labeled oligodendrocytes supplying processes to the proximal region of the axon. These experiments indicated that the axon initial segment was ϳ40 m in length, and the first node of Ranvier was ϳ90 m from the axon hillock. Experiments targeting the first node of Ranvier suggested it was not involved in action potential initiation. In conclusion, these results indicate that, in layer 5 pyramidal neurons, action potentials are generated in the distal region of the axon initial segment.

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Section: Development Of Action Potential Initiation and Propagationmentioning

confidence: 99%

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

2006

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“…This saltatory propagation permits a significant increase in the velocity of the action potential propagating along the axon (Fig. 6.11) (Huxley and Stämpfli, 1949;Stämpfli, 1954;Bishop and Levick, 1956;Fitzhugh, 1962;Stämpfli, 1983;Terakawa and Hsu, 1991). …”

Section: Interpretation Of the Action Potential As A Depolarization Wavementioning

confidence: 99%

Integrated Molecular and Cellular Biophysics

Raicu

Popescu

2008

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“…Myelin is a modified plasma membrane of oligodendrocytes in the CNS, which enwraps a segment of axon in a spiral fashion ( Barres et al, 1993 ). Myelination affects function and molecular organization of axons allowing faster signal propagation with reduced energy consumption ( Frankenhaeuser and Schneider, 1951 ; Bishop and Levick, 1956 ; Homma et al, 1983 ; Saab et al, 2013 ; Stiefel et al, 2013 ). Several proteins in myelin have been identified to play essential roles in axonal maintenance and function.…”

Section: Normal Molecular Organization Of Myelin and Nodes Of Ranviermentioning

confidence: 99%

Myelin damage and repair in pathologic CNS: challenges and prospects

Alizadeh

Dyck

Karimi-Abdolrezaee

2015

Front. Mol. Neurosci.

184

148

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Injury to the central nervous system (CNS) results in oligodendrocyte cell death and progressive demyelination. Demyelinated axons undergo considerable physiological changes and molecular reorganizations that collectively result in axonal dysfunction, degeneration and loss of sensory and motor functions. Endogenous adult oligodendrocyte precursor cells and neural stem/progenitor cells contribute to the replacement of oligodendrocytes, however, the extent and quality of endogenous remyelination is suboptimal. Emerging evidence indicates that optimal remyelination is restricted by multiple factors including (i) low levels of factors that promote oligodendrogenesis; (ii) cell death among newly generated oligodendrocytes, (iii) inhibitory factors in the post-injury milieu that impede remyelination, and (iv) deficient expression of key growth factors essential for proper re-construction of a highly organized myelin sheath. Considering these challenges, over the past several years, a number of cell-based strategies have been developed to optimize remyelination therapeutically. Outcomes of these basic and preclinical discoveries are promising and signify the importance of remyelination as a mechanism for improving functions in CNS injuries. In this review, we provide an overview on: (1) the precise organization of myelinated axons and the reciprocal axo-myelin interactions that warrant properly balanced physiological activities within the CNS; (2) underlying cause of demyelination and the structural and functional consequences of demyelination in axons following injury and disease; (3) the endogenous mechanisms of oligodendrocyte replacement; (4) the modulatory role of reactive astrocytes and inflammatory cells in remyelination; and (5) the current status of cell-based therapies for promoting remyelination. Careful elucidation of the cellular and molecular mechanisms of demyelination in the pathologic CNS is a key to better understanding the impact of remyelination for CNS repair.

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Saltatory conduction in single isolated and non‐isolated myelinated nerve fibres

Cited by 10 publications

References 15 publications

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

Integrated Molecular and Cellular Biophysics

Myelin damage and repair in pathologic CNS: challenges and prospects

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