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: 31 December 2024 | Viewed by 1028

Special Issue Editors


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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
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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
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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

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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 (1 paper)

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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
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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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