Abstract
Nerve impulses travel along myelinated axons as much as 300-fold faster than they do along unmyelinated axons. Myelination is essential for normal nervous system behavior in vertebrates as illustrated by leukodystrophies, such as amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS), where myelin is degenerated or damaged. The increased conduction velocity that occurs in myelinated axons is dependent on gaps in the myelin called Nodes of Ranvier that are enriched in ion channels. These Nodes are separated by long stretches of myelin insulation where no transmembrane ion conductance occurs. It is believed that the action potential jumps or skips between nodes, conserving its information content, while maintaining its speed. In this study, a model is presented that implicates Nodes of Ranvier as responsible for regenerating the proton hopping that is responsible for nerve impulse conductance in myelinated axons.
Keywords: Action potential, information flow, nerve impulses, node of Ranvier, proton hopping.
Current Computer-Aided Drug Design
Title:Enhanced Action Potential Passage Through the Node of Ranvier of Myelinated Axons via Proton Hopping
Volume: 11 Issue: 1
Author(s): Lemont Kier, Lowell Hall and Robert M. Tombes
Affiliation:
Keywords: Action potential, information flow, nerve impulses, node of Ranvier, proton hopping.
Abstract: Nerve impulses travel along myelinated axons as much as 300-fold faster than they do along unmyelinated axons. Myelination is essential for normal nervous system behavior in vertebrates as illustrated by leukodystrophies, such as amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS), where myelin is degenerated or damaged. The increased conduction velocity that occurs in myelinated axons is dependent on gaps in the myelin called Nodes of Ranvier that are enriched in ion channels. These Nodes are separated by long stretches of myelin insulation where no transmembrane ion conductance occurs. It is believed that the action potential jumps or skips between nodes, conserving its information content, while maintaining its speed. In this study, a model is presented that implicates Nodes of Ranvier as responsible for regenerating the proton hopping that is responsible for nerve impulse conductance in myelinated axons.
Export Options
About this article
Cite this article as:
Kier Lemont, Hall Lowell and Tombes M. Robert, Enhanced Action Potential Passage Through the Node of Ranvier of Myelinated Axons via Proton Hopping, Current Computer-Aided Drug Design 2015; 11 (1) . https://dx.doi.org/10.2174/157340991101150722142734
DOI https://dx.doi.org/10.2174/157340991101150722142734 |
Print ISSN 1573-4099 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6697 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
A Clinical View of BDNF-TrkB Signaling in the Treatment of Major Depression
Current Signal Transduction Therapy Integrating Qualitative and Quantitative Tools for the Detection and Identification of Lectins in Major Human Diseases
Protein & Peptide Letters Novel Indications for Benzodiazepine Antagonist Flumazenil in GABA Mediated Pathological Conditions of the Central Nervous System
Current Pharmaceutical Design Adenosine and ATP Receptors in the Brain
Current Topics in Medicinal Chemistry Targeting Mitochondrial Dysfunction in Chronic Heart Failure: Current Evidence and Potential Approaches
Current Pharmaceutical Design The Role of local Insulin-like Growth Factor-1 Isoforms in the Pathophysiology of Skeletal Muscle
Current Genomics Recent Advances in Neuroinflammation Therapeutics: PPARs/LXR as Neuroinflammatory Modulators
Current Pharmaceutical Design Melatonin and Its Therapeutic Potential in Neuroprotection
Central Nervous System Agents in Medicinal Chemistry Review of Recent Clinical Developments and Patents for the Treatment of Autoimmune and Inflammatory Diseases by Mesenchymal Stromal Cells
Recent Patents on Regenerative Medicine Neuronal High-Affinity Sodium-Dependent Glutamate Transporters (EAATs): Targets for the Development of Novel Therapeutics Against Neurodegenerative Diseases
Current Pharmaceutical Design Old Friends in New Constellations - the Hematopoetic Growth Factors G-CSF, GMCSF, and EPO for the Treatment of Neurological Diseases
Current Medicinal Chemistry Spin Trapping: An Essential Tool for the Study of Diseases Caused by Oxidative Stress
Current Topics in Medicinal Chemistry Bioinformatics and Protein Design
Current Pharmaceutical Biotechnology Programmed Cell Death Mechanisms in Neurological Disease
Current Molecular Medicine Intracellular Calcium Homeostasis and Kidney Disease
Current Medicinal Chemistry Nanoneuromedicines for Neurodegenerative Diseases
Nanoscience & Nanotechnology-Asia Potential Therapeutic Targets for Neurodegenerative Diseases: Lessons Learned from Calorie Restriction
Current Drug Targets Virus-Based RNA Silencing Agents and Virus-Derived Expression Vectors as Gene Therapy Vehicles
Recent Patents on Biotechnology Emerging Evidence for the Role of Neurotransmitters in the Modulation of T Cell Responses to Cognate Ligands
Central Nervous System Agents in Medicinal Chemistry Neuroinflammation and Neuroprotection: An Update on (Future) Neurotrophin-Related Strategies in Multiple Sclerosis Treatment
Current Medicinal Chemistry