The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
W. A. Jacak - One of the best experts on this subject based on the ideXlab platform.
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New wave-type mechanism of Saltatory Conduction in myelinated axons and micro-Saltatory Conduction in C fibres
European Biophysics Journal, 2020Co-Authors: J. E. Jacak, W. A. JacakAbstract:We present a new wave-type model of Saltatory Conduction in myelinated axons. Poor conductivity in the neuron cytosol limits electrical current signal velocity according to cable theory, to 1–3 m/s, whereas Saltatory Conduction occurs with a velocity of 100–300 m/s. We propose a wave-type mechanism for Saltatory Conduction in the form of the kinetics of an ionic plasmon-polariton being the hybrid of the electro-magnetic wave and of the synchronized ionic plasma oscillations in myelinated segments along an axon. The model agrees with observations and allows for description of the regulatory role of myelin. It explains also the mechanism of Conduction deficiency in demyelination syndromes such as multiple sclerosis. The recently observed micro-Saltatory Conduction in ultrathin unmyelinated C fibers with periodic ion gate clusters is also explained.
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ion plasmon collective oscillations underlying Saltatory Conduction in myelinated axons and topological homotopy concept of memory
2020Co-Authors: W. A. Jacak, J. E. JacakAbstract:Abstract We demonstrate a new wave-type model of Saltatory Conduction in myelinated axons. A poor conductivity of the neuron cytosol limits electrical current signal velocity upon the cable theory, to 1–3 m/s, whereas the Saltatory Conduction undergoes with the velocity of signal transduction 100–300 m/s. We propose the wave-type mechanism of the Saltatory Conduction in the form of kinetics of ion plasmon-polariton being the hybrid of the electromagnetic wave and of the ion plasma oscillations, which meets the observations. Plasmons oscillations have a quantum character to some extent as the coherent oscillations of all ions are possible due to their repulsion which can be understood upon the quantum approach like random phase approximation by Pines and Bohm. Basing on the difference of electricity of myelinated white matter and nonmyelinated gray matter in cortex we outline the topological concept of the memory functioning.
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new plasmon polariton model of the Saltatory Conduction
bioRxiv, 2020Co-Authors: W. A. JacakAbstract:We propose a new model of the Saltatory Conduction in myelinated axons. This Conduction of the action potential in myelinated axons does not agree with the conventional cable theory, though the latter has satisfactorily explained the electrosignaling in dendrites and in unmyelinated axons. By the development of the wave-type concept of ionic plasmon-polariton kinetics in axon cytosol we have achieved an agreement of the model with observed properties of the Saltatory Conduction. Some resulting consequences of the different electricity model in the white and the gray matter for nervous system organization have been also outlined. SIGNIFICANCEMost of axons in peripheral nervous system and in white matter of brain and spinal cord are myelinated with the action potential kinetics speed two orders greater than in dendrites and in unmyelinated axons. A decrease of the Saltatory Conduction velocity by only 10% ceases body functioning. Conventional cable theory, useful for dendrites and unmyelinated axon, does not explain the Saltatory Conduction (discrepancy between the speed assessed and the observed one is of one order of the magnitude). We propose a new nonlocal collective mechanism of ion density oscillations synchronized in the chain of myelinated segments of plasmon-polariton type, which is consistent with observations. This model explains the role of the myelin in other way than was previously thought.
Jack Rosenbluth - One of the best experts on this subject based on the ideXlab platform.
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axon glia interactions and the domain organization of myelinated axons requires neurexin iv caspr paranodin
Neuron, 2001Co-Authors: Manzoor A Bhat, Jose C Rios, Yue Lu, German P Garciafresco, William Ching, Mary St Martin, Jingjun Li, Steven Einheber, Mitchell Chesler, Jack RosenbluthAbstract:Abstract Myelinated fibers are organized into distinct domains that are necessary for Saltatory Conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K + channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve Conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal Saltatory Conduction.
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Axon-Glia Interactions and the Domain Organization of Myelinated Axons Requires Neurexin IV/Caspr/Paranodin
Neuron, 2001Co-Authors: Manzoor A Bhat, Jose C Rios, Yue Lu, William Ching, Mary St Martin, Jingjun Li, Steven Einheber, Mitchell Chesler, German P. Garcia-fresco, Jack RosenbluthAbstract:Abstract Myelinated fibers are organized into distinct domains that are necessary for Saltatory Conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K + channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve Conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal Saltatory Conduction.
Susumu Terakawa - One of the best experts on this subject based on the ideXlab platform.
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experimental confirmation of the Saltatory Conduction hypothesis
2013Co-Authors: Ke Xu, Susumu TerakawaAbstract:In Chap. 7, we learned the hypothesis of Saltatory Conduction was based on the experiments by Tasaki et al. in the toad single myelinated fiber preparation. It was immediately supported by new experiments in the frog single myelinated fiber preparation by Huxley and Stampfli (1949). Then, Stampfli (1954), in a review, proposed three conditions for the experimental proof of the hypothesis of Saltatory Conduction. There were a few investigators who objected to the Saltatory Conduction hypothesis and insisted that the nerve impulse was also continuously conducted under the myelin sheath as a pass-through tunnel (Lorente de No and Honrubia 1964, 1965). At the present time, Saltatory Conduction in the myelinated fibers of vertebrates has been adopted by most neurobiologists and is included as a subject in most texts and reference books of neurobiology. Nevertheless, Saltatory Conduction as reported in the nervous system of the Penaeus shrimp in invertebrates is not yet commonly introduced in the neurobiological literature. In view of these circumstances, the Saltatory Conduction hypothesis needs to be thoroughly confirmed by experiments. Fortunately, the myelinated giant fiber of the Penaeus shrimp can be used as a suitable preparation for this purpose. Namely, the wide submyelinic space of the giant fiber can be considered as a “wide natural tunnel” between the myelin sheath and axon in the myelinated fibers. Moreover, its long internodal distance is advantageous for experimental operation. Making the best use of these properties in the giant fiber preparation of the Penaeus shrimp, the three conditions for the proof of the Saltatory Conduction hypothesis proposed by Stampfli (1954) were all fulfilled.
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Saltatory Conduction found in the nervous system of two model invertebrates the shrimp penaeus and the earthworm lumbricus terrestris
2013Co-Authors: Ke Xu, Susumu TerakawaAbstract:As already described, the finding of the Saltatory Conduction phenomenon in the nervous system of a few invertebrate animals was mentioned in some neurobiological literature, but a conclusion on the lack of Saltatory Conduction in the nervous system of invertebrates had not yet been generally revised. The reason for this seemed to be that a Saltatory Conduction in invertebrates is based on the functional spots, which could not be accepted as a true node. Therefore, before presenting the experimental findings that demonstrate the phenomenon of Saltatory Conduction in the nervous system of invertebrates, it is necessary to discuss the common understanding of the true nodal structure of the myelinated fibers.
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fenestration in the myelin sheath of nerve fibers of the shrimp a novel node of excitation for Saltatory Conduction
Journal of Neurobiology, 1996Co-Authors: Susumu TerakawaAbstract:Giant nerve fibers of the shrimp family Penaeidae conduct impulses at the velocity highest among all animal species (∼210 m/s; highest in mammals = 120 m/s). We examined these giant and other small nerve fibers morphologically using a differential interference contrast microscope as well as an electron microscope, and found a very specialized form of excitable membrane that functions as a node for Saltatory Conduction of the impulse. This node appeared under the light microscope as a characteristic pattern of concentrically aligned rings in a very small spot of the myelin sheath. The diameter of the innermost ring of the node was about 5 μm, and the distance between these nodes was as long as 12 mm. Via an electron microscope, these nodes were characterized by a complete lack of the myelin sheath, forming a fenestration that has a tight junction with an axonal membrane. Voltage clamp measurements by a sucrose gap technique demonstrated that the axonal membrane at these fenestration nodes is exclusively excitable and that the large submyelinic space is a unique conductive pathway for loop currents for Saltatory Conduction through such fenestration nodes. © 1996 John Wiley & Sons, Inc.
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Saltatory Conduction and a novel type of excitable fenestra in shrimp myelinated nerve fibers
Japanese Journal of Physiology, 1993Co-Authors: Ke Xu, Susumu TerakawaAbstract:: The findings of Saltatory Conduction in the invertebrate giant nerve fibers were mentioned, and the experiments for analyzing the mechanism of impulse Conduction in the giant myelinated nerve fibers of Penaeus orientalis and Penaeus japonicus were reviewed. Saltatory Conduction was also found in many middle- and small-sized myelinated nerve fibers of, at least, 6 species of Penaeus shrimps. Saltatory Conduction with its morphological basis in myelinated nerve fibers of vertebrates and invertebrates were compared, and it was concluded that the myelination of the nerve fibers in vertebrates and invertebrates has occurred independently.
Matthew N. Rasband - One of the best experts on this subject based on the ideXlab platform.
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Saltatory Conduction jumping to new conclusions
Current Biology, 2020Co-Authors: Matthew N. RasbandAbstract:Summary Rapid and efficient Saltatory action potential Conduction depends on the myelin sheath and clustered Na+ channels at nodes of Ranvier. A new study convincingly shows that the periaxonal space is a necessary conductive component to accurately model myelinated axon physiology and Saltatory Conduction.
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Glial regulation of the axonal membrane at nodes of Ranvier.
Current Opinion in Neurobiology, 2006Co-Authors: Dorothy P. Schafer, Matthew N. RasbandAbstract:Action potential Conduction in myelinated nerve fibers depends on a polarized axonal membrane. Voltage-gated Na+ and K+ channels are clustered at nodes of Ranvier and mediate the transmembrane currents necessary for rapid Saltatory Conduction. Paranodal junctions flank nodes and function as attachment sites for myelin and as paracellular and membrane protein diffusion barriers. Common molecular mechanisms, directed by myelinating glia, are used to establish these axonal membrane domains. Initially, heterophilic interactions between glial and axonal cell adhesion molecules define the locations where nodes or paranodes form. Subsequently, within each domain, axonal cell adhesion molecules are stabilized and retained through interactions with cytoskeletal and scaffolding proteins, including ankyrins and spectrins.
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eLS - Myelin and Action Potential Propagation
Encyclopedia of Life Sciences, 2001Co-Authors: Matthew N. RasbandAbstract:The high action potential Conduction velocities achieved in some vertebrate axons are a consequence of myelin, an insulating sheath made by glial cells, and clustered sodium ion (Na+) channels found at regularly spaced gaps in the myelin sheath. Keywords: node of Ranvier; Saltatory Conduction; myelin; Na+ channels; glia
Jun Kimura - One of the best experts on this subject based on the ideXlab platform.
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the physiological effect of anti gm1 antibodies on Saltatory Conduction and transmembrane currents in single motor axons
Brain, 1997Co-Authors: Nobuyuki Hirota, Ryuji Kaji, Hugh Bostock, Katsuro Shindo, Teruaki Kawasaki, Kotaro Mizutani, Nobuo Kohara, Takahiko Saida, Jun KimuraAbstract:Anti-ganglioside (anti-GM1) antibodies have been implicated in the pathogenesis of Guillain-Barre syndrome, multifocal motor neuropathy and motor neuron diseases. It has been held that they may interfere with Saltatory Conduction by blocking sodium channels. We tested this hypothesis by analysing action potentials from 140 single nerve fibres in 22 rat ventral roots using external longitudinal current measurement. High-titre anti-GM1 sera from Guillain-Barre syndrome or multifocal motor neuropathy patients, or anti-GM1 rabbit sera were applied to the rat ventral root, where Saltatory Conduction in single motor fibres was serially observed for 4-12 h (mean 8.2 h). For control experiments, we also tested anti-galactocerebroside (anti-GalC) sera, which causes acute demyelinative Conduction block, and tetrodotoxin (TTX), a sodium channel blocker. Conduction block was found in 82% of the fibres treated with anti-GalC sera and 100% treated with TTX, but only in 2% (one out of 44) treated with the patients' sera and 5% (two out of 38) treated with rabbit anti-GM1 sera. All the nodes blocked by anti-GM1 sera revealed intense passive outward membrane current, in the internode just beyond the last active node. This pattern of current flow was similar to that in fibres blocked by demyelination with anti-GalC sera, and quite different from that seen in fibres blocked by reducing sodium currents with TTX. Our findings suggest that anti-GM1 sera neither mediate Conduction block nor block sodium channels on their own. We conclude that physiological action of the antibody alone is insufficient to explain clinically observed Conduction block in human diseases.
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The physiological effect of anti-GM1 antibodies on Saltatory Conduction and transmembrane currents in single motor axons.
Brain : a journal of neurology, 1997Co-Authors: Nobuyuki Hirota, Ryuji Kaji, Hugh Bostock, Katsuro Shindo, Teruaki Kawasaki, Kotaro Mizutani, Nobuo Kohara, Takahiko Saida, Jun KimuraAbstract:Anti-ganglioside (anti-GM1) antibodies have been implicated in the pathogenesis of Guillain-Barré syndrome, multifocal motor neuropathy and motor neuron diseases. It has been held that they may interfere with Saltatory Conduction by blocking sodium channels. We tested this hypothesis by analysing action potentials from 140 single nerve fibres in 22 rat ventral roots using external longitudinal current measurement. High-titre anti-GM1 sera from Guillain-Barré syndrome or multifocal motor neuropathy patients, or anti-GM1 rabbit sera were applied to the rat ventral root, where Saltatory Conduction in single motor fibres was serially observed for 4-12 h (mean 8.2 h). For control experiments, we also tested anti-galactocerebroside (anti-GalC) sera, which causes acute demyelinative Conduction block, and tetrodotoxin (TTX), a sodium channel blocker. Conduction block was found in 82% of the fibres treated with anti-GalC sera and 100% treated with TTX, but only in 2% (one out of 44) treated with the patients' sera and 5% (two out of 38) treated with rabbit anti-GM1 sera. All the nodes blocked by anti-GM1 sera revealed intense passive outward membrane current, in the internode just beyond the last active node. This pattern of current flow was similar to that in fibres blocked by demyelination with anti-GalC sera, and quite different from that seen in fibres blocked by reducing sodium currents with TTX. Our findings suggest that anti-GM1 sera neither mediate Conduction block nor block sodium channels on their own. We conclude that physiological action of the antibody alone is insufficient to explain clinically observed Conduction block in human diseases.
