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Biomolecules
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Nerve Conduction Inhibition to Alleviate Disease Symptoms: Clinical Drugs and...
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Nerve Conduction Inhibition to Alleviate Disease Symptoms: Clinical Drugs and Medicinal Plant Compounds

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1530

Special Issue Editor

Dr. Eiichi Kumamoto

E-Mail Website
Guest Editor
Emeritus Professor, Saga University, Saga, Japan
Interests: nerve conduction; synaptic transmission; synaptic plasticity; pain; neuron; spinal dorsal horn; sciatic nerve; glutamate receptor; GABA receptor; glycine receptor; TRP channel; analgesic; plant-derived compound; electrophysiology; patch-clamp

Special Issue Information

Dear Colleagues,

Neuronal information is transmitted from the periphery to higher centers by action potential (AP) conduction in nerve fibers and chemical transmission at synapses. Although synaptic transmission is modified by drugs that alleviate various disease symptoms, nerve AP conduction is also a target for the drugs. For instance, there are anesthetics, analgesics, antiepileptics, and antidepressants that inhibit nerve conduction.  Even NSAIDs inhibit nerve conduction. Likely, drugs used in folk medicine, many of which are derived from plants, also suppress nerve conduction. Nerve conduction inhibitors have the ability to modulate TRP channels that are involved in sensory transmission, cancer progression, and so on. Nerve conduction inhibition is mainly due to a modulation of voltage-gated sodium and potassium channels that are involved in AP production. It is highly likely that the specific structures of a drug capable of inhibiting nerve conduction are involved in a modulation of activation of the channels. Studies to clarify the chemical structures and mechanisms of the modulation involved and to find new clinical and plant-derived compounds for nerve conduction inhibition are necessary to identify therapeutically effective drugs. We invite authors to submit original research manuscripts, reviews, and communications related to any of these aspects.

Dr. Eiichi Kumamoto
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nerve conduction
  • action potential
  • clinical drug
  • medicinal plant compound
  • voltage-gated ion channel

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Published Papers (1 paper)

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Review

23 pages, 512 KiB  
Review
Anesthetic- and Analgesic-Related Drugs Modulating Both Voltage-Gated Na+ and TRP Channels
by Eiichi Kumamoto
Biomolecules 2024, 14(12), 1619; https://doi.org/10.3390/biom14121619 - 18 Dec 2024
Cited by 1 | Viewed by 1128
Abstract
Nociceptive information is transmitted by action potentials (APs) through primary afferent neurons from the periphery to the central nervous system. Voltage-gated Na+ channels are involved in this AP production, while transient receptor potential (TRP) channels, which are non-selective cation channels, are involved [...] Read more.
Nociceptive information is transmitted by action potentials (APs) through primary afferent neurons from the periphery to the central nervous system. Voltage-gated Na+ channels are involved in this AP production, while transient receptor potential (TRP) channels, which are non-selective cation channels, are involved in receiving and transmitting nociceptive stimuli in the peripheral and central terminals of the primary afferent neurons. Peripheral terminal TRP vanilloid-1 (TRPV1), ankylin-1 (TRPA1) and melastatin-8 (TRPM8) activation produces APs, while central terminal TRP activation enhances the spontaneous release of L-glutamate from the terminal to spinal cord and brain stem lamina II neurons that play a pivotal role in modulating nociceptive transmission. There is much evidence demonstrating that chemical compounds involved in Na+ channel (or nerve AP conduction) inhibition modify TRP channel functions. Among these compounds are local anesthetics, anti-epileptics, α2-adrenoceptor agonists, antidepressants (all of which are used as analgesic adjuvants), general anesthetics, opioids, non-steroidal anti-inflammatory drugs and plant-derived compounds, many of which are involved in antinociception. This review mentions the modulation of Na+ channels and TRP channels including TRPV1, TRPA1 and TRPM8, both of which modulations are produced by pain-related compounds. Full article
(This article belongs to the Special Issue Nerve Conduction Inhibition to Alleviate Disease Symptoms: Clinical Drugs and Medicinal Plant Compounds)
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