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Neuronal Voltage-Gated Channel Regulation
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Neuronal Voltage-Gated Channel Regulation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 7244

Special Issue Editors

Dr. Dax A. Hoffman

E-Mail Website
Guest Editor
Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA
Interests: dendrites; intrinsic excitability; learning and memory; synaptic plasticity; hippocampus; ion channels; voltage-gated potassium channels; neuronal development; Autism
Dr. Jonathan G. Murphy

E-Mail Website
Guest Editor
Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA
Interests: voltage-gated ion channels; calcium signaling; synaptic plasticity; fragile X syndrome; potassium channel interacting proteins; ion channel regulation by post transcriptional modifications

Special Issue Information

Dear Colleagues,

Neuronal voltage-gated ion channels (nVGICs) control neuronal excitability and plasticity. Regulation of ion channel function by post-translational modifications and/or channel-associated regulatory proteins affect their expression, biophysical properties, subcellular localization, trafficking, and subsequent intracellular signaling.  Inherited mutations affecting nVGICs or their regulation produce channel-based pathologies or “channelopathies” that affect the central nervous system including epilepsy, Fragile X syndrome, ataxia, and pain syndromes. Dysregulation of nVGICs is also strongly associated with pathophysiology in central nervous system disorders affecting memory and mental illness.  This special issue focusses on channel physiology with an emphasis on the diverse means by which nVGIC function is regulated. nVGICs are themselves frequent drug targets but greater understanding of their regulation may lead to new tool development providing a vital, more subtle resource for future therapeutics.

Dr. Dax A. Hoffman
Dr. Jonathan G. Murphy
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • voltage-gated ion channel
  • post-translational modifications
  • auxiliary subunits
  • excitability
  • ion channel regulation
  • channelopathies
  • tools for ion channel research
  • ion channel pharmacology

Published Papers (3 papers)

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Research

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17 pages, 1847 KiB  
Article
Inhibition of the Akt/PKB Kinase Increases Nav1.6-Mediated Currents and Neuronal Excitability in CA1 Hippocampal Pyramidal Neurons
by Mate Marosi, Miroslav N. Nenov, Jessica Di Re, Nolan M. Dvorak, Musaad Alshammari and Fernanda Laezza
Int. J. Mol. Sci. 2022, 23(3), 1700; https://doi.org/10.3390/ijms23031700 - 01 Feb 2022
Cited by 6 | Viewed by 2057
Abstract
In neurons, changes in Akt activity have been detected in response to the stimulation of transmembrane receptors. However, the mechanisms that lead to changes in neuronal function upon Akt inhibition are still poorly understood. In the present study, we interrogate how Akt inhibition [...] Read more.
In neurons, changes in Akt activity have been detected in response to the stimulation of transmembrane receptors. However, the mechanisms that lead to changes in neuronal function upon Akt inhibition are still poorly understood. In the present study, we interrogate how Akt inhibition could affect the activity of the neuronal Nav channels with while impacting intrinsic excitability. To that end, we employed voltage-clamp electrophysiological recordings in heterologous cells expressing the Nav1.6 channel isoform and in hippocampal CA1 pyramidal neurons in the presence of triciribine, an inhibitor of Akt. We showed that in both systems, Akt inhibition resulted in a potentiation of peak transient Na+ current (INa) density. Akt inhibition correspondingly led to an increase in the action potential firing of the CA1 pyramidal neurons that was accompanied by a decrease in the action potential current threshold. Complementary confocal analysis in the CA1 pyramidal neurons showed that the inhibition of Akt is associated with the lengthening of Nav1.6 fluorescent intensity along the axonal initial segment (AIS), providing a mechanism for augmented neuronal excitability. Taken together, these findings provide evidence that Akt-mediated signal transduction might affect neuronal excitability in a Nav1.6-dependent manner. Full article
(This article belongs to the Special Issue Neuronal Voltage-Gated Channel Regulation)
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Review

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24 pages, 2306 KiB  
Review
Neuronal Roles of the Multifunctional Protein Dipeptidyl Peptidase-like 6 (DPP6)
by Cole Malloy, Maisie Ahern, Lin Lin and Dax A. Hoffman
Int. J. Mol. Sci. 2022, 23(16), 9184; https://doi.org/10.3390/ijms23169184 - 16 Aug 2022
Cited by 4 | Viewed by 2187
Abstract
The concerted action of voltage-gated ion channels in the brain is fundamental in controlling neuronal physiology and circuit function. Ion channels often associate in multi-protein complexes together with auxiliary subunits, which can strongly influence channel expression and function and, therefore, neuronal computation. One [...] Read more.
The concerted action of voltage-gated ion channels in the brain is fundamental in controlling neuronal physiology and circuit function. Ion channels often associate in multi-protein complexes together with auxiliary subunits, which can strongly influence channel expression and function and, therefore, neuronal computation. One such auxiliary subunit that displays prominent expression in multiple brain regions is the Dipeptidyl aminopeptidase-like protein 6 (DPP6). This protein associates with A-type K+ channels to control their cellular distribution and gating properties. Intriguingly, DPP6 has been found to be multifunctional with an additional, independent role in synapse formation and maintenance. Here, we feature the role of DPP6 in regulating neuronal function in the context of its modulation of A-type K+ channels as well as its independent involvement in synaptic development. The prevalence of DPP6 in these processes underscores its importance in brain function, and recent work has identified that its dysfunction is associated with host of neurological disorders. We provide a brief overview of these and discuss research directions currently underway to advance our understanding of the contribution of DPP6 to their etiology. Full article
(This article belongs to the Special Issue Neuronal Voltage-Gated Channel Regulation)
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19 pages, 1668 KiB  
Review
Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function
by Nicholas C. Vierra and James S. Trimmer
Int. J. Mol. Sci. 2022, 23(4), 1953; https://doi.org/10.3390/ijms23041953 - 10 Feb 2022
Cited by 4 | Viewed by 2317
Abstract
The concerted function of the large number of ion channels expressed in excitable cells, including brain neurons, shapes diverse signaling events by controlling the electrical properties of membranes. It has long been recognized that specific groups of ion channels are functionally coupled in [...] Read more.
The concerted function of the large number of ion channels expressed in excitable cells, including brain neurons, shapes diverse signaling events by controlling the electrical properties of membranes. It has long been recognized that specific groups of ion channels are functionally coupled in mediating ionic fluxes that impact membrane potential, and that these changes in membrane potential impact ion channel gating. Recent studies have identified distinct sets of ion channels that can also physically and functionally associate to regulate the function of either ion channel partner beyond that afforded by changes in membrane potential alone. Here, we review canonical examples of such ion channel partnerships, in which a Ca2+ channel is partnered with a Ca2+-activated K+ channel to provide a dedicated route for efficient coupling of Ca2+ influx to K+ channel activation. We also highlight examples of non-canonical ion channel partnerships between Ca2+ channels and voltage-gated K+ channels that are not intrinsically Ca2+ sensitive, but whose partnership nonetheless yields enhanced regulation of one or the other ion channel partner. We also discuss how these ion channel partnerships can be shaped by the subcellular compartments in which they are found and provide perspectives on how recent advances in techniques to identify proteins in close proximity to one another in native cells may lead to an expanded knowledge of other ion channel partnerships. Full article
(This article belongs to the Special Issue Neuronal Voltage-Gated Channel Regulation)
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