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Ion Channels in the Nervous System
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Ion Channels in the Nervous System

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: 20 February 2025 | Viewed by 10141

Special Issue Editor

Dr. Hana Zemkova

E-Mail Website
Guest Editor
Institute of Physiology, Czech Academy of Sciences, 14220 Prague, Czech Republic
Interests: release of neurotransmitters and hormones; ion channels; P2X receptors; molecular structure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ion channels are fundamentally involved in most neuronal functions, and their abnormal functioning plays a role in a number of disorders and diseased states often accompanied by neurodegeneration in the central and peripheral nervous systems. Understanding the processes regulating the trafficking and functioning of ion channels in the brain is crucial for developing new therapeutic strategies for the wide variety of channelopathies and neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease, as well as for neuropathic pain states that manifest neuronal damage. In this Special Issue, original studies or review articles on all aspects of trafficking and functioning of voltage-gated and ligand-gated ion channels (Na+, K+, Ca2+, and Cl- channels, and ionotrophic glutamate- and GABA-gated and purinergic P2X receptor channels, for example) expressed in neurons and glia cells are welcome. In particular, molecular analyses of their structure and function, ion selectivity, localization, physiology, and pharmacology, as well as the impact of novel screening technologies on understanding neuronal activity in vivo, are favorable. It will also cover the reports providing new insights into modeling the diversity of spontaneous and agonist-induced patterns of action potentials.

Dr. Hana Zemkova
Guest Editor

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Keywords

  • voltage-gated ion channels
  • ligand-gated ion channels
  • neurons
  • glia cells
  • electrical activity
  • molecular structure
  • molecular pathway

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Published Papers (5 papers)

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Research

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10 pages, 9070 KiB  
Article
Glucocorticoids Selectively Inhibit Hippocampal CA1 Pyramidal Neurons Activity Through HCN Channels
by Chenyang Li, Tongchuang Lu, Chengfang Pan and Changlong Hu
Int. J. Mol. Sci. 2024, 25(22), 11971; https://doi.org/10.3390/ijms252211971 - 7 Nov 2024
Viewed by 837
Abstract
Glucocorticoids are known to influence hippocampal function, but their rapid non-genomic effects on specific neurons in the hippocampal trisynaptic circuit remain underexplored. This study investigated the immediate effects of glucocorticoids on CA1 and CA3 pyramidal neurons, and dentate gyrus (DG) granule neurons in [...] Read more.
Glucocorticoids are known to influence hippocampal function, but their rapid non-genomic effects on specific neurons in the hippocampal trisynaptic circuit remain underexplored. This study investigated the immediate effects of glucocorticoids on CA1 and CA3 pyramidal neurons, and dentate gyrus (DG) granule neurons in rats using the patch-clamp technique. We found that a 5 min extracellular application of corticosterone significantly reduced action potential firing frequency in CA1 pyramidal neurons, while no effects were observed in CA3 or DG neurons. The corticosterone-induced inhibition in CA1 was blocked by the glucocorticoid receptor antagonist CORT125281, but remained unaffected by the mineralocorticoid receptor antagonist spironolactone. Notably, membrane-impermeable bovine serum albumin-conjugated dexamethasone mimicked corticosterone’s effects on CA1 neurons, which exhibited prominent hyperpolarization-activated cyclic nucleotide-gated (HCN) channel currents. Pyramidal neurons in CA3 and granular neurons in the DG showed little HCN channel currents. Corticosterone enhanced HCN channel activity in CA1 neurons via glucocorticoid receptors, and the HCN channel inhibitor ZD7288 abolished corticosterone’s suppressive effects on action potentials. These findings suggest that glucocorticoids selectively inhibit CA1 pyramidal neuron activity through HCN channels, providing new insight into the mechanisms of glucocorticoid action in hippocampal circuits. Full article
(This article belongs to the Special Issue Ion Channels in the Nervous System)
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15 pages, 4881 KiB  
Article
Eicosapentaenoic Acid Modulates Transient Receptor Potential V1 Expression in Specific Brain Areas in a Mouse Fibromyalgia Pain Model
by Hsien-Yin Liao, Chia-Ming Yen, I-Han Hsiao, Hsin-Cheng Hsu and Yi-Wen Lin
Int. J. Mol. Sci. 2024, 25(5), 2901; https://doi.org/10.3390/ijms25052901 - 1 Mar 2024
Cited by 5 | Viewed by 1579
Abstract
Pain is an unpleasant sensory and emotional experience accompanied by tissue injury. Often, an individual’s experience can be influenced by different physiological, psychological, and social factors. Fibromyalgia, one of the most difficult-to-treat types of pain, is characterized by general muscle pain accompanied by [...] Read more.
Pain is an unpleasant sensory and emotional experience accompanied by tissue injury. Often, an individual’s experience can be influenced by different physiological, psychological, and social factors. Fibromyalgia, one of the most difficult-to-treat types of pain, is characterized by general muscle pain accompanied by obesity, fatigue, sleep, and memory and psychological concerns. Fibromyalgia increases nociceptive sensations via central sensitization in the brain and spinal cord level. We used intermittent cold stress to create a mouse fibromyalgia pain model via a von Frey test (day 0: 3.69 ± 0.14 g; day 5: 2.13 ± 0.12 g). Mechanical pain could be reversed by eicosapentaenoic acid (EPA) administration (day 0: 3.72 ± 0.14 g; day 5: 3.69 ± 0.13 g). A similar trend could also be observed for thermal hyperalgesia. The levels of elements in the transient receptor potential V1 (TRPV1) signaling pathway were increased in the ascending pain pathway, including the thalamus, medial prefrontal cortex, somatosensory cortex, anterior cingulate cortex, and cerebellum. EPA intake significantly attenuated this overexpression. A novel chemogenetics method was used to inhibit SSC and ACC activities, which presented an analgesic effect through the TRPV1 downstream pathway. The present results provide insights into the role of the TRPV1 signaling pathway for fibromyalgia and its potential as a clinical target. Full article
(This article belongs to the Special Issue Ion Channels in the Nervous System)
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Review

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21 pages, 835 KiB  
Review
Ion Channels in Odor Information Processing of Neural Circuits of the Vertebrate Olfactory Bulb
by Yunqing Yu, Ping Liao and Ruotian Jiang
Int. J. Mol. Sci. 2024, 25(24), 13259; https://doi.org/10.3390/ijms252413259 - 10 Dec 2024
Viewed by 689
Abstract
Olfactory disorders and their associated complications present a considerable challenge to an individual’s quality of life and emotional wellbeing. The current range of treatments, including surgical procedures, pharmacological interventions, and behavioral training, frequently proves ineffective in restoring olfactory function. The olfactory bulb (OB) [...] Read more.
Olfactory disorders and their associated complications present a considerable challenge to an individual’s quality of life and emotional wellbeing. The current range of treatments, including surgical procedures, pharmacological interventions, and behavioral training, frequently proves ineffective in restoring olfactory function. The olfactory bulb (OB) is essential for odor processing and plays a pivotal role in the development of these disorders. Despite the acknowledged significance of ion channels in sensory functions and related pathologies, their specific involvement in OB remains unexplored. This review presents an overview of the functions of various ion channel families in regulating neuronal excitability, synaptic transmission, and the complex processes of olfactory perception. The objective of this review was to elucidate the role of ion channels in olfactory function, providing new insights into the diagnosis and treatment of olfactory dysfunction. Full article
(This article belongs to the Special Issue Ion Channels in the Nervous System)
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22 pages, 880 KiB  
Review
Pathological Functions of Lysosomal Ion Channels in the Central Nervous System
by Jianke Cen, Nan Hu, Jiawen Shen, Yongjing Gao and Huanjun Lu
Int. J. Mol. Sci. 2024, 25(12), 6565; https://doi.org/10.3390/ijms25126565 - 14 Jun 2024
Cited by 1 | Viewed by 2408
Abstract
Lysosomes are highly dynamic organelles that maintain cellular homeostasis and regulate fundamental cellular processes by integrating multiple metabolic pathways. Lysosomal ion channels such as TRPML1-3, TPC1/2, ClC6/7, CLN7, and TMEM175 mediate the flux of Ca2+, Cl−, Na+, [...] Read more.
Lysosomes are highly dynamic organelles that maintain cellular homeostasis and regulate fundamental cellular processes by integrating multiple metabolic pathways. Lysosomal ion channels such as TRPML1-3, TPC1/2, ClC6/7, CLN7, and TMEM175 mediate the flux of Ca2+, Cl−, Na+, H+, and K+ across lysosomal membranes in response to osmotic stimulus, nutrient-dependent signals, and cellular stresses. These ion channels serve as the crucial transducers of cell signals and are essential for the regulation of lysosomal biogenesis, motility, membrane contact site formation, and lysosomal homeostasis. In terms of pathophysiology, genetic variations in these channel genes have been associated with the development of lysosomal storage diseases, neurodegenerative diseases, inflammation, and cancer. This review aims to discuss the current understanding of the role of these ion channels in the central nervous system and to assess their potential as drug targets. Full article
(This article belongs to the Special Issue Ion Channels in the Nervous System)
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20 pages, 3410 KiB  
Review
Ion Channel Disturbances in Migraine Headache: Exploring the Potential Role of the Kynurenine System in the Context of the Trigeminovascular System
by Eleonóra Spekker, Gábor Nagy-Grócz and László Vécsei
Int. J. Mol. Sci. 2023, 24(23), 16574; https://doi.org/10.3390/ijms242316574 - 21 Nov 2023
Cited by 7 | Viewed by 3898
Abstract
Migraine is a primary headache disorder, which is an enormous burden to the healthcare system. While some aspects of the pathomechanism of migraines remain unknown, the most accepted theory is that activation and sensitization of the trigeminovascular system are essential during migraine attacks. [...] Read more.
Migraine is a primary headache disorder, which is an enormous burden to the healthcare system. While some aspects of the pathomechanism of migraines remain unknown, the most accepted theory is that activation and sensitization of the trigeminovascular system are essential during migraine attacks. In recent decades, it has been suggested that ion channels may be important participants in the pathogenesis of migraine. Numerous ion channels are expressed in the peripheral and central nervous systems, including the trigeminovascular system, affecting neuron excitability, synaptic energy homeostasis, inflammatory signaling, and pain sensation. Dysfunction of ion channels could result in neuronal excitability and peripheral or central sensitization. This narrative review covers the current understanding of the biological mechanisms leading to activation and sensitization of the trigeminovascular pain pathway, with a focus on recent findings on ion channel activation and modulation. Furthermore, we focus on the kynurenine pathway since this system contains kynurenic acid, which is an endogenous glutamate receptor antagonist substance, and it has a role in migraine pathophysiology. Full article
(This article belongs to the Special Issue Ion Channels in the Nervous System)
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