Calcium Signaling in Neurons and Glial Cells: Role of Cav1 channels

Alves, Vitor S.; Alves-Silva, Hélio S; Orts, Diego J. B.; Ribeiro‐Silva, Luisa; Arcísio-Miranda, Manoel; Oliveira, Fernando A.

doi:10.1016/j.neuroscience.2019.09.041

Cited by 19 publications

(17 citation statements)

References 217 publications

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“…The pore-forming α1-subunit determines channel activity, whereas other subunits are auxiliary and regulate function of α1-subunit. In mammalian cells, 10 different α1-subunits, encoded by different genes, classify into three subfamilies: Ca V 1, Ca V 2, and Ca V 3 (Catterall, 2011 ; Zamponi et al, 2015 ; Alves et al, 2019 ). Depending on the pharmacological properties and activation voltage of Ca 2+ currents, five different types of VGCCs are distinguished: L-type, N-type, P/Q-type, R-type, and T-type.…”

Section: K + Channelsmentioning

confidence: 99%

“…Ca V 1.2 channels account for 89% of all Ca 2+ currents mediated by L-type VGCCs in the brain (Alves et al, 2019 ; Enders et al, 2020 ). In hippocampal neurons, Ca V 1.2 channels localize to somatodendritic compartment being placed at synapses or extra-synaptically (Joux et al, 2001 ; Hoogland and Saggau, 2004 ; Obermair et al, 2004 ; Tippens et al, 2008 ; Ortner and Striessnig, 2016 ), as well as to axons and/or extrasynaptic regions of axonal terminals (Tippens et al, 2008 ).…”

Section: K + Channelsmentioning

confidence: 99%

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Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Boscia

Elkjaer

Illés

et al. 2021

Front. Cell. Neurosci.

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Despite significant advances in our understanding of the pathophysiology of multiple sclerosis (MS), knowledge about contribution of individual ion channels to axonal impairment and remyelination failure in progressive MS remains incomplete. Ion channel families play a fundamental role in maintaining white matter (WM) integrity and in regulating WM activities in axons, interstitial neurons, glia, and vascular cells. Recently, transcriptomic studies have considerably increased insight into the gene expression changes that occur in diverse WM lesions and the gene expression fingerprint of specific WM cells associated with secondary progressive MS. Here, we review the ion channel genes encoding K+, Ca2+, Na+, and Cl− channels; ryanodine receptors; TRP channels; and others that are significantly and uniquely dysregulated in active, chronic active, inactive, remyelinating WM lesions, and normal-appearing WM of secondary progressive MS brain, based on recently published bulk and single-nuclei RNA-sequencing datasets. We discuss the current state of knowledge about the corresponding ion channels and their implication in the MS brain or in experimental models of MS. This comprehensive review suggests that the intense upregulation of voltage-gated Na+ channel genes in WM lesions with ongoing tissue damage may reflect the imbalance of Na+ homeostasis that is observed in progressive MS brain, while the upregulation of a large number of voltage-gated K+ channel genes may be linked to a protective response to limit neuronal excitability. In addition, the altered chloride homeostasis, revealed by the significant downregulation of voltage-gated Cl− channels in MS lesions, may contribute to an altered inhibitory neurotransmission and increased excitability.

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Section: K + Channelsmentioning

confidence: 99%

Section: K + Channelsmentioning

confidence: 99%

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Boscia

Elkjaer

Illés

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…In neurons, Ca 2+ plays a dual role as a charge carrier and ubiquitous second messenger. This dual nature allows for the generation of a broad spectrum of signals, which can be distinguished by spatial and temporal dimensions, amplitude, frequency of oscillations or localization to discrete neuronal compartments [10][11][12][13]. The readout of these signals by local or global Ca 2+ -sensing proteins and subsequent transmission of decoded message to cellular effectors underlies the involvement of calcium in a wide range of crucial generic process, such as apoptosis, gene transcription or proliferation.…”

Section: Ca 2+ Homeostasis In Healthy Neuronsmentioning

confidence: 99%

Ketamine and Calcium Signaling—A Crosstalk for Neuronal Physiology and Pathology

Lisek

Żylińska

Boczek

2020

IJMS

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Ketamine is a non-competitive antagonist of NMDA (N-methyl-D-aspartate) receptor, which has been in clinical practice for over a half century. Despite recent data suggesting its harmful side effects, such as neuronal loss, synapse dysfunction or disturbed neural network formation, the drug is still applied in veterinary medicine and specialist anesthesia. Several lines of evidence indicate that structural and functional abnormalities in the nervous system caused by ketamine are crosslinked with the imbalanced activity of multiple Ca2+-regulated signaling pathways. Due to its ubiquitous nature, Ca2+ is also frequently located in the center of ketamine action, although the precise mechanisms underlying drug’s negative or therapeutic properties remain mysterious for the large part. This review seeks to delineate the relationship between ketamine-triggered imbalance in Ca2+ homeostasis and functional consequences for downstream processes regulating key aspects of neuronal function.

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“…So far, there has been no model addressing the unique features of astrocyte. Based on our previous model [4] and the literature reported data [5][6][7][8], we have implemented the relatively comprehensive simulations on Ca 2+ oscillations in astrocytes mediated by A  Methods on the simulation In the model astrocyte (see Figure 1), different types of voltage-gated calcium channels (VGCCs) [5] form the Ca 2+ influx J VGCC from the extracellular space (ECS) to the intracellular space (ICS). The electrophysiological properties of these VGCCs were described by the Hodgkin-Huxley (HH) equations.…”

Section: Introductionmentioning

confidence: 99%

“…The electrophysiological properties of these VGCCs were described by the Hodgkin-Huxley (HH) equations. Only the L-type VGCC current may be medicated by A [6]To investigate the effects of Aβ, we use parameter  to represent a fixed level of Aβ concentration presenting in the environment. This parameter is also used in the following equations.…”

Section: Introductionmentioning

confidence: 99%

Simulation of Ca²⁺oscillations in astrocytes mediated by amyloid beta in Alzheimer’s disease

Gao

Liu

Chen

2020

Preprint

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Disruptions of astrocyte Ca 2+ signaling is important in Alzheimer's disease (AD) with the unclear mechanism of amyloid beta peptide (A). We have modified our previous computational model of spontaneous Ca 2+ oscillations in astrocytes to investigate the effects of Aon intracellular Ca 2+ dynamics. The simulation results have shown consistence with the previous experiments. Acan increase the resting concentration of intracellular Ca 2+ and change the regime of Ca 2+ oscillations by activating L-type voltage-gated calcium channels and the metabolic glutamate receptors, or by increasing ryanodine receptors sensitivity and Ca 2+ leakage, respectively. This work have provided a toolkit to study the influence of Aon intracellular Ca 2+ dynamics in AD. It is helpful for understanding the toxic role of Aduring the progression of AD. Statement of SignificanceAlzheimer's disease (AD) is the most common neurodegenerative disease with the unclear mechanism of amyloid beta peptide (A). This work have implemented a computational model to address the Ca 2+ dynamics of astrocyte mediated by Awith the four different pathways: voltage-gated calcium channels, metabotropic glutamate receptors 5, ryanodine receptor channels and membrane leak. The Ca 2+ oscillations and bifurcation diagram indicate that astrocytes exhibit ionic excitability mediated by Aβ and become the potential targets of Aneurotoxicity. We expect this shared computational model would advance the understanding of AD.

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Calcium Signaling in Neurons and Glial Cells: Role of Cav1 channels

Cited by 19 publications

References 217 publications

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Ketamine and Calcium Signaling—A Crosstalk for Neuronal Physiology and Pathology

Simulation of Ca²⁺oscillations in astrocytes mediated by amyloid beta in Alzheimer’s disease

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Calcium Signaling in Neurons and Glial Cells: Role of Cav1 channels

Cited by 19 publications

References 217 publications

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?

Ketamine and Calcium Signaling—A Crosstalk for Neuronal Physiology and Pathology

Simulation of Ca2+oscillations in astrocytes mediated by amyloid beta in Alzheimer’s disease

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Product

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Simulation of Ca²⁺oscillations in astrocytes mediated by amyloid beta in Alzheimer’s disease