Neuronal Blocking Factors in Demyelinating Diseases

Theodore Cummins, Stephen G. Waxman

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

This chapter discusses the role of various conduction blocking factors in multiple sclerosis and other inflammatory diseases. It is noted that conduction block which results from demyelination and axonal degeneration contribute to the production of clinical deficits in experimental models of demyelinating disease and in multiple sclerosis (MS), Guillain-Barré syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy. A variety of putative blocking factors have been proposed over the last four decades including antibodies, cytokines, small peptides, and nitric oxide. Many of these blocking factors that have been investigated are thought to target voltage-gated sodium channels. Several mechanisms by which drugs and other factors can reduce the activity of voltage-gated sodium channels have been identified. Some biological toxins, such as tetrodotoxin, directly block sodium currents by binding in the pore of the channel and preventing the flow of sodium ions through the pore. Furthermore, modulation of other channels or membrane proteins might also contribute to block of impulse transmission, most of the work on the role of blocking factors in inflammatory demyelinating diseases has focused on voltage-gated sodium channels.

Original languageEnglish
Title of host publicationMultiple Sclerosis as A Neuronal Disease
PublisherElsevier Inc.
Pages317-326
Number of pages10
ISBN (Print)9780127387611
DOIs
StatePublished - 2005

Fingerprint

Demyelinating Diseases
Voltage-Gated Sodium Channels
Multiple Sclerosis
Biological Toxins
Sodium
Chronic Inflammatory Demyelinating Polyradiculoneuropathy
Tetrodotoxin
Nitric Oxide
Membrane Proteins
Theoretical Models
Ions
Cytokines
Peptides
blocking factor
Antibodies
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Dentistry(all)
  • Medicine(all)

Cite this

Cummins, T., & Waxman, S. G. (2005). Neuronal Blocking Factors in Demyelinating Diseases. In Multiple Sclerosis as A Neuronal Disease (pp. 317-326). Elsevier Inc.. https://doi.org/10.1016/B978-012738761-1/50023-7

Neuronal Blocking Factors in Demyelinating Diseases. / Cummins, Theodore; Waxman, Stephen G.

Multiple Sclerosis as A Neuronal Disease. Elsevier Inc., 2005. p. 317-326.

Research output: Chapter in Book/Report/Conference proceedingChapter

Cummins, T & Waxman, SG 2005, Neuronal Blocking Factors in Demyelinating Diseases. in Multiple Sclerosis as A Neuronal Disease. Elsevier Inc., pp. 317-326. https://doi.org/10.1016/B978-012738761-1/50023-7
Cummins T, Waxman SG. Neuronal Blocking Factors in Demyelinating Diseases. In Multiple Sclerosis as A Neuronal Disease. Elsevier Inc. 2005. p. 317-326 https://doi.org/10.1016/B978-012738761-1/50023-7
Cummins, Theodore ; Waxman, Stephen G. / Neuronal Blocking Factors in Demyelinating Diseases. Multiple Sclerosis as A Neuronal Disease. Elsevier Inc., 2005. pp. 317-326
@inbook{6bc71241593345fe922b95f052b4deb9,
title = "Neuronal Blocking Factors in Demyelinating Diseases",
abstract = "This chapter discusses the role of various conduction blocking factors in multiple sclerosis and other inflammatory diseases. It is noted that conduction block which results from demyelination and axonal degeneration contribute to the production of clinical deficits in experimental models of demyelinating disease and in multiple sclerosis (MS), Guillain-Barr{\'e} syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy. A variety of putative blocking factors have been proposed over the last four decades including antibodies, cytokines, small peptides, and nitric oxide. Many of these blocking factors that have been investigated are thought to target voltage-gated sodium channels. Several mechanisms by which drugs and other factors can reduce the activity of voltage-gated sodium channels have been identified. Some biological toxins, such as tetrodotoxin, directly block sodium currents by binding in the pore of the channel and preventing the flow of sodium ions through the pore. Furthermore, modulation of other channels or membrane proteins might also contribute to block of impulse transmission, most of the work on the role of blocking factors in inflammatory demyelinating diseases has focused on voltage-gated sodium channels.",
author = "Theodore Cummins and Waxman, {Stephen G.}",
year = "2005",
doi = "10.1016/B978-012738761-1/50023-7",
language = "English",
isbn = "9780127387611",
pages = "317--326",
booktitle = "Multiple Sclerosis as A Neuronal Disease",
publisher = "Elsevier Inc.",

}

TY - CHAP

T1 - Neuronal Blocking Factors in Demyelinating Diseases

AU - Cummins, Theodore

AU - Waxman, Stephen G.

PY - 2005

Y1 - 2005

N2 - This chapter discusses the role of various conduction blocking factors in multiple sclerosis and other inflammatory diseases. It is noted that conduction block which results from demyelination and axonal degeneration contribute to the production of clinical deficits in experimental models of demyelinating disease and in multiple sclerosis (MS), Guillain-Barré syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy. A variety of putative blocking factors have been proposed over the last four decades including antibodies, cytokines, small peptides, and nitric oxide. Many of these blocking factors that have been investigated are thought to target voltage-gated sodium channels. Several mechanisms by which drugs and other factors can reduce the activity of voltage-gated sodium channels have been identified. Some biological toxins, such as tetrodotoxin, directly block sodium currents by binding in the pore of the channel and preventing the flow of sodium ions through the pore. Furthermore, modulation of other channels or membrane proteins might also contribute to block of impulse transmission, most of the work on the role of blocking factors in inflammatory demyelinating diseases has focused on voltage-gated sodium channels.

AB - This chapter discusses the role of various conduction blocking factors in multiple sclerosis and other inflammatory diseases. It is noted that conduction block which results from demyelination and axonal degeneration contribute to the production of clinical deficits in experimental models of demyelinating disease and in multiple sclerosis (MS), Guillain-Barré syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy. A variety of putative blocking factors have been proposed over the last four decades including antibodies, cytokines, small peptides, and nitric oxide. Many of these blocking factors that have been investigated are thought to target voltage-gated sodium channels. Several mechanisms by which drugs and other factors can reduce the activity of voltage-gated sodium channels have been identified. Some biological toxins, such as tetrodotoxin, directly block sodium currents by binding in the pore of the channel and preventing the flow of sodium ions through the pore. Furthermore, modulation of other channels or membrane proteins might also contribute to block of impulse transmission, most of the work on the role of blocking factors in inflammatory demyelinating diseases has focused on voltage-gated sodium channels.

UR - http://www.scopus.com/inward/record.url?scp=84882538016&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84882538016&partnerID=8YFLogxK

U2 - 10.1016/B978-012738761-1/50023-7

DO - 10.1016/B978-012738761-1/50023-7

M3 - Chapter

AN - SCOPUS:84882538016

SN - 9780127387611

SP - 317

EP - 326

BT - Multiple Sclerosis as A Neuronal Disease

PB - Elsevier Inc.

ER -