*Result*: Distinctive Properties and Powerful Neuromodulation of Na v 1.6 Sodium Channels Regulates Neuronal Excitability.
Title:
Distinctive Properties and Powerful Neuromodulation of Na v 1.6 Sodium Channels Regulates Neuronal Excitability.
Authors:
Zybura A; Program in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Biology Department, School of Science, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA., Hudmon A; Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN 47907, USA., Cummins TR; Program in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Biology Department, School of Science, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Source:
Cells [Cells] 2021 Jun 25; Vol. 10 (7). Date of Electronic Publication: 2021 Jun 25.
Publication Type:
Journal Article; Research Support, N.I.H., Extramural; Review
Language:
English
Journal Info:
Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI
MeSH Terms:
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Grant Information:
U54 NS108874 United States NS NINDS NIH HHS; R33 DA041876 United States DA NIDA NIH HHS
Contributed Indexing:
Keywords: action potential; axon initial segment; channelopathies; post-translational modifications; protein-protein interactions; sodium currents; voltage-gated sodium channel
Substance Nomenclature:
0 (Calmodulin)
0 (NAV1.6 Voltage-Gated Sodium Channel)
SY7Q814VUP (Calcium)
0 (NAV1.6 Voltage-Gated Sodium Channel)
SY7Q814VUP (Calcium)
Entry Date(s):
Date Created: 20210702 Date Completed: 20211026 Latest Revision: 20250104
Update Code:
20260130
PubMed Central ID:
PMC8307729
DOI:
10.3390/cells10071595
PMID:
34202119
Database:
MEDLINE
*Further Information*
*Voltage-gated sodium channels (Navs) are critical determinants of cellular excitability. These ion channels exist as large heteromultimeric structures and their activity is tightly controlled. In neurons, the isoform Na <subscript>v</subscript> 1.6 is highly enriched at the axon initial segment and nodes, making it critical for the initiation and propagation of neuronal impulses. Changes in Na <subscript>v</subscript> 1.6 expression and function profoundly impact the input-output properties of neurons in normal and pathological conditions. While mutations in Na <subscript>v</subscript> 1.6 may cause channel dysfunction, aberrant changes may also be the result of complex modes of regulation, including various protein-protein interactions and post-translational modifications, which can alter membrane excitability and neuronal firing properties. Despite decades of research, the complexities of Na <subscript>v</subscript> 1.6 modulation in health and disease are still being determined. While some modulatory mechanisms have similar effects on other Nav isoforms, others are isoform-specific. Additionally, considerable progress has been made toward understanding how individual protein interactions and/or modifications affect Na <subscript>v</subscript> 1.6 function. However, there is still more to be learned about how these different modes of modulation interact. Here, we examine the role of Na <subscript>v</subscript> 1.6 in neuronal function and provide a thorough review of this channel's complex regulatory mechanisms and how they may contribute to neuromodulation.*