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Pharmaceuticals
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Calcium Channels as Therapeutic Targets
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Calcium Channels as Therapeutic Targets

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 2189

Special Issue Editors

Prof. Dr. Gary J. Stephens

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Guest Editor
School of Pharmacy, University of Reading, Whiteknights, PO Box 228, Reading RG6 6AJ, UK
Interests: electrophysiology; voltage-gated calcium channels; cannabinoids; ion channels; GPCRs; pain; ataxia
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. David Adams

E-Mail Website
Guest Editor
Illawarra Health and Medical Research Institute (IHMRI), University of Wollongong, Wollongong, NSW 2522, Australia
Interests: acetylcholine nicotinic receptors; voltage-gated ion channels; venom peptides; conotoxins; structure-function relationship; electrophysiology; nociception
Special Issues, Collections and Topics in MDPI journals
Dr. Hussein N. Rubaiy

E-Mail Website
Guest Editor
Department of Laboratory Medicine, Division of Clinical Pharmacology, Karolinska Institute & Karolinska University Hospital, C1:68, 141 86 Stockholm, Sweden
Interests: calcium channels; TRPC channels; ion channels
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ion channels are key modulators of intracellular levels of Ca2+, which, in turn, is a vital physiological ‘second messenger’. Whether modulated through voltage changes, endogenous ligands/protein partners, and/or changes to Ca2+ levels, different Ca2+ channel families represent key molecular targets in a range of pathophysiologies that carry a heavy health, well-being, and economic burden. Thus, Ca2+ channels are major targets in diseases, including pain, epilepsy, neurodegenerative disorders, and neuropsychiatric disorders. Understanding and treating these diseases is increasingly relevant in today’s aging society.

This Special Issue will shed light on new pharmacological agents that modulate different classes of Ca2+ channels, including voltage-gated and transient receptor potential channels and/or the auxiliary subunits that make up the protein complex. We welcome submissions from diverse fields of studies, including, but not limited to, the development of small molecular entities and biological drugs, the development of toxins from the plant and animal kingdoms, the exploitation of knowledge of Ca2+ channel structure and function, and genetic studies of channelopathies and disease association.

Prof. Dr. Gary J. Stephens
Prof. Dr. David Adams
Dr. Hussein N. Rubaiy
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. Pharmaceuticals 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 2900 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

  • voltage-gated Ca2+ channels
  • TRP channels
  • Ca2+-permeable TRP and ASIC channels
  • STIM/orai channels
  • Ca2+ channel structure and function
  • Ca2+ channel toxins
  • Ca2+ channelopathies
  • neuropharmacology
  • pain
  • epilepsy
  • neurodegenerative and neuropsychiatric disorders

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Published Papers (2 papers)

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28 pages, 5414 KiB  
Article
Autism-Linked Mutations in α2δ-1 and α2δ-3 Reduce Protein Membrane Expression but Affect Neither Calcium Channels nor Trans-Synaptic Signaling
by Sabrin Haddad, Manuel Hessenberger, Cornelia Ablinger, Clarissa Eibl, Ruslan Stanika, Marta Campiglio and Gerald J. Obermair
Pharmaceuticals 2024, 17(12), 1608; https://doi.org/10.3390/ph17121608 - 28 Nov 2024
Viewed by 696
Abstract
Background: α2δ proteins regulate membrane trafficking and biophysical properties of voltage-gated calcium channels. Moreover, they modulate axonal wiring, synapse formation, and trans-synaptic signaling. Several rare missense variants in CACNA2D1 (coding for α2δ-1) and CACNA2D3 (coding for α2δ-3) [...] Read more.
Background: α2δ proteins regulate membrane trafficking and biophysical properties of voltage-gated calcium channels. Moreover, they modulate axonal wiring, synapse formation, and trans-synaptic signaling. Several rare missense variants in CACNA2D1 (coding for α2δ-1) and CACNA2D3 (coding for α2δ-3) genes were identified in patients with autism spectrum disorder (ASD). However, the pathogenicity of these variants is not known, and the molecular mechanism by which α2δ proteins may contribute to the pathophysiology of autism is, as of today, not understood. Therefore, in this study we functionally characterized two heterozygous missense variants in α2δ-1 (p.R351T) and α2δ-3 (p.A275T), previously identified in patients with ASD. Methods: Electrophysiological recordings in transfected tsA201 cells were used to study specific channel-dependent functions of mutated α2δ proteins. Membrane expression, presynaptic targeting, and trans-synaptic signaling of mutated α2δ proteins were studied upon expression in murine cultured hippocampal neurons. Results: Homologous expression of both mutated α2δ proteins revealed a strongly reduced membrane expression and synaptic localization compared to the corresponding wild type α2δ proteins. Moreover, the A275T mutation in α2δ-3 resulted in an altered glycosylation pattern upon heterologous expression. However, neither of the mutations compromised the biophysical properties of postsynaptic L-type (CaV1.2 and CaV1.3) and presynaptic P/Q-type (CaV2.1) channels when co-expressed in tsA201 cells. Furthermore, presynaptic expression of p.R351T in the α2δ-1 splice variant lacking exon 23 did not affect trans-synaptic signaling to postsynaptic GABAA receptors. Conclusions: Our data provide evidence that the pathophysiological mechanisms of ASD-causing mutations of α2δ proteins may not involve their classical channel-dependent and trans-synaptic functions. Alternatively, these mutations may induce subtle changes in synapse formation or neuronal network function, highlighting the need for future α2δ protein-linked disease models. Full article
(This article belongs to the Special Issue Calcium Channels as Therapeutic Targets)
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8 pages, 1306 KiB  
Brief Report
Rat Sympathetic Neuron Calcium Channels Are Insensitive to Gabapentin
by Mallory B. Scott and Paul J. Kammermeier
Pharmaceuticals 2024, 17(9), 1237; https://doi.org/10.3390/ph17091237 - 19 Sep 2024
Viewed by 859
Abstract
The gabapentenoids such as gabapentin (GP) and pregabalin are approved for the treatment of chronic pain, but their utility is limited by persistent side effects. These adverse effects result from GPs affecting many types of neurons and muscle cells, not just the pain-sensing [...] Read more.
The gabapentenoids such as gabapentin (GP) and pregabalin are approved for the treatment of chronic pain, but their utility is limited by persistent side effects. These adverse effects result from GPs affecting many types of neurons and muscle cells, not just the pain-sensing neurons that are the intended targets. We have recently discovered a type of peripheral neuron, rat sympathetic neurons from the superior cervical ganglion (SCG), that is uniquely insensitive to GP effects. Currents were measured using whole-cell patch-clamp electrophysiology from cells in primary culture from either the SCG or the Nodose Ganglion (NDG) as a positive control for the effects of GP. We find that the calcium current density was dramatically reduced by GP pretreatment in NDG neurons, but that neurons from the SCG were resistant. Further, when GP was cytoplasmically injected into these neurons, the resistance of SCG neurons to GP treatment persisted. These data demonstrate that rat sympathetic neurons appear to be uniquely resistant to GP treatment. These results may help us to better understand the mechanism of action of, and resistance to, GP in altering calcium channel current density, which may help to develop future treatments with fewer side effects. Full article
(This article belongs to the Special Issue Calcium Channels as Therapeutic Targets)
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