Neuronal excitability: membrane ion channels

2002 ◽  
pp. 35-52
Keyword(s):  
Ion Channels ◽  
Neuronal Excitability

scholarly journals Acid sensing ion channels regulate neuronal excitability by inhibiting BK potassium channels

2012 ◽  
Vol 426 (4) ◽  
pp. 511-515 ◽  
Author(s):  
Elena Petroff ◽  
Vladislav Snitsarev ◽  
Huiyu Gong ◽  
Francois M. Abboud
Keyword(s):  
Ion Channels ◽  
Potassium Channels ◽  
Neuronal Excitability ◽  
Acid Sensing Ion Channels

The Voltage-Dependent K+ Channel Family

2019 ◽  
Author(s):  
Hanne B. Rasmussen ◽  
James S. Trimmer
Keyword(s):  
Ion Channels ◽  
Neuronal Excitability ◽  
Expression Patterns ◽  
Basic Knowledge ◽  
K Channel ◽  
Dependent Manner ◽  
Kv Channels ◽  
Voltage Dependent ◽  
The Individual ◽  
Α Subunits

Voltage-dependent K+ (potassium; Kv) channels are ion channels that critically impact neuronal excitability and function. Four principal α subunits assemble to create a membrane-spanning pore that opens in a voltage-dependent manner to allow the selective passage of K+ ions across the cell membrane. Forty human genes encoding Kv channel α subunits have been identified, and most of them are expressed in the nervous system. The individual Kv subunits display unique cellular and subcellular expression patterns and co-assemble into distinct homo- and hetero-tetrameric channels that differ in their electrophysiological and pharmacological properties, and their sensitivity to dynamic modulation, by cellular signaling pathways. The resulting diversity allows Kv channels to impact all steps in electrical information processing, as well as numerous other aspects of neuronal functions, including those in which they appear to play a non-conducting role. This chapter reviews the current basic knowledge about this large and important family of ion channels.

Acclimatory-phase specificity of gene expression during the course of heat acclimation and superimposed hypohydration in the rat hypothalamus

2006 ◽  
Vol 100 (6) ◽  
pp. 1992-2003 ◽  
Author(s):  
Hagit Schwimmer ◽  
Luba Eli-Berchoer ◽  
Michal Horowitz
Keyword(s):  
Ion Channels ◽  
Neuronal Excitability ◽  
Heat Acclimation ◽  
Metabolic Efficiency ◽  
Gene Profiles ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Labeled Rna ◽  
Regulatory Functions ◽  
Functional Analyses

The induction of the heat-acclimated phenotype involves reprogramming the expression of genes encoding both constitutive and inducible proteins. In this investigation, we studied the global genomic response in the hypothalamus during heat acclimation, with and without combined hypohydration stress. Rats were acclimated for 2 days (STHA) or for 30 days (LTHA) at 34°C. Hypohydration (10% decrease in body weight) was attained by water deprivation. 32P-labeled RNA samples from the hypothalamus were hybridized onto cDNA Atlas array (Clontech no. 1.2) membranes. Clustering and functional analyses of the expression profile of a battery of genes representing various central regulatory functions of body homeostasis demonstrated a biphasic acclimation profile with a transient upregulation of genes encoding ion channels, transporters, and transmitter signaling upon STHA. After LTHA, most genes returned to their preacclimation expression levels. In both STHA and LTHA, genes encoding hormones and neuropeptides, linked with metabolic rate and food intake, were downregulated. This genomic profile, demonstrating an enhanced transcription of genes linked with neuronal excitability during STHA and enhanced metabolic efficiency upon LTHA, is consistent with our previously established integrative acclimation model. The response to hypohydration was characterized by an upregulation of a large number of genes primarily associated with the regulation of ion channels, cell volume, and neuronal excitability. During STHA, the response was transiently desensitized, recovering upon LTHA. We conclude that hypohydration overrides the heat acclimatory status. It is notable that STHA and hypohydration gene profiles are analogous with the physiological profile described in the response to various types of brain injury.

scholarly journals Electrophysiological Profile Remodeling via Selective Suppression of Voltage-Gated Currents by CLN1/PPT1 Overexpression in Human Neuronal-Like Cells

2020 ◽  
Vol 14 ◽  
Author(s):  
Gian Carlo Demontis ◽  
Francesco Pezzini ◽  
Elisa Margari ◽  
Marzia Bianchi ◽  
Biancamaria Longoni ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Neuronal Excitability ◽  
Membrane Conductance ◽  
Premature Death ◽  
Resting Potential ◽  
Voltage Gated ◽  
Transcriptomic Data ◽  
Voltage Gated Ion Channels ◽  
Gated Ion Channels

CLN1 disease (OMIM #256730) is an inherited neurological disorder of early childhood with epileptic seizures and premature death. It is associated with mutations in CLN1 coding for Palmitoyl-Protein Thioesterase 1 (PPT1), a lysosomal enzyme which affects the recycling and degradation of lipid-modified (S-acylated) proteins by removing palmitate residues. Transcriptomic evidence from a neuronal-like cellular model derived from differentiated SH-SY5Y cells disclosed the potential negative roles of CLN1 overexpression, affecting the elongation of neuronal processes and the expression of selected proteins of the synaptic region. Bioinformatic inquiries of transcriptomic data pinpointed a dysregulated expression of several genes coding for proteins related to voltage-gated ion channels, including subunits of calcium and potassium channels (VGCC and VGKC). In SH-SY5Y cells overexpressing CLN1 (SH-CLN1 cells), the resting potential and the membrane conductance in the range of voltages close to the resting potential were not affected. However, patch-clamp recordings indicated a reduction of Ba2+ currents through VGCC of SH-CLN1 cells; Ca2+ imaging revealed reduced Ca2+ influx in the same cellular setting. The results of the biochemical and morphological investigations of CACNA2D2/α2δ-2, an accessory subunit of VGCC, were in accordance with the downregulation of the corresponding gene and consistent with the hypothesis that a lower number of functional channels may reach the plasma membrane. The combined use of 4-AP and NS-1643, two drugs with opposing effects on Kv11 and Kv12 subfamilies of VGKC coded by the KCNH gene family, provides evidence for reduced functional Kv12 channels in SH-CLN1 cells, consistent with transcriptomic data indicating the downregulation of KCNH4. The lack of compelling evidence supporting the palmitoylation of many ion channels subunits investigated in this study stimulates inquiries about the role of PPT1 in the trafficking of channels to the plasma membrane. Altogether, these results indicate a reduction of functional voltage-gated ion channels in response to CLN1/PPT1 overexpression in differentiated SH-SY5Y cells and provide new insights into the altered neuronal excitability which may underlie the severe epileptic phenotype of CLN1 disease. It remains to be shown if remodeling of such functional channels on plasma membrane can occur as a downstream effect of CLN1 disease.

scholarly journals Using the Patch-Clamp technique to shed light on ion channels structure, function and pharmacology

2014 ◽  
Author(s):  
Roberta Gualdani
Keyword(s):  
Ion Channels ◽  
Patch Clamp ◽  
Transient Receptor Potential ◽  
Neuronal Excitability ◽  
Receptor Potential ◽  
Cellular Membrane ◽  
Bk Channel ◽  
K Channel ◽  
Patch Clamp Technique ◽  
Transient Receptor

Ion channels are membrane proteins that selectively allow ions to flow down their electrochemical gradient across the cellular membrane. They localize in both plasma and intracellular membranes and regulate a variety of functions such as neuronal excitability, heartbeat, muscle contraction and hormones release. Thus, understanding the molecular mechanism of ion channels function and regulation is one of the key goals of modern Biophysics. During my PhD thesis, by combining patch-clamp measurements with site-direct mutagenesis, fluorophore labeling experiments and pharmacological assays, I explored some functional and structural properties of different ion transporters: the Na+/Ca2+ exchanger (NCX); the large conductance Ca2+-voltage activated K+ channel (BK) channel; the human Transient receptor potential, member A1 (TRPA1) channel.

scholarly journals Serum-deprived differentiated neuroblastoma F-11 cells express functional dorsal root ganglion neuron properties

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7951 ◽  
Author(s):  
Valentina Pastori ◽  
Alessia D’Aloia ◽  
Stefania Blasa ◽  
Marzia Lecchi
Keyword(s):  
Ion Channels ◽  
Dorsal Root Ganglion ◽  
Electrical Activity ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Calcium Currents ◽  
High Threshold ◽  
Drg Neurons ◽  
Proximal Urethra

The isolation and culture of dorsal root ganglion (DRG) neurons cause adaptive changes in the expression and regulation of ion channels, with consequences on neuronal excitability. Considering that not all neurons survive the isolation and that DRG neurons are heterogeneous, it is difficult to find the cellular subtype of interest. For this reason, researchers opt for DRG-derived immortal cell lines to investigate endogenous properties. The F-11 cell line is a hybridoma of embryonic rat DRG neurons fused with the mouse neuroblastoma line N18TG2. In the proliferative condition, F-11 cells do not display a gene expression profile correspondent with specific subclasses of sensory neurons, but the most significant differences when compared with DRGs are the reduction of voltage-gated sodium, potassium and calcium channels, and the small amounts of TRPV1 transcripts. To investigate if functional properties of mature F-11 cells showed more similarities with those of isolated DRG neurons, we differentiated them by serum deprivation. Potassium and sodium currents significantly increased with differentiation, and biophysical properties of tetrodotoxin (TTX)-sensitive currents were similar to those characterized in small DRG neurons. The analysis of the voltage-dependence of calcium currents demonstrated the lack of low threshold activated components. The exclusive expression of high threshold activated Ca2+ currents and of TTX-sensitive Na+ currents correlated with the generation of a regular tonic electrical activity, which was recorded in the majority of the cells (80%) and was closely related to the activity of afferent TTX-sensitive A fibers of the proximal urethra and the bladder. Responses to capsaicin and substance P were also recorded in ~20% and ~80% of cells, respectively. The percentage of cells responsive to acetylcholine was consistent with the percentage referred for rat DRG primary neurons and cell electrical activity was modified by activation of non-NMDA receptors as for embryonic DRG neurons. These properties and the algesic profile (responses to pH5 and sensitivity to both ATP and capsaicin), proposed in literature to define a sub-classification of acutely dissociated rat DRG neurons, suggest that differentiated F-11 cells express receptors and ion channels that are also present in sensory neurons.

scholarly journals HCN3 ion channels: roles in sensory neuronal excitability and pain

2019 ◽  
Vol 597 (17) ◽  
pp. 4661-4675 ◽  
Author(s):  
Sergio Lainez ◽  
Christoforos Tsantoulas ◽  
Martin Biel ◽  
Peter A McNaughton
Keyword(s):  
Ion Channels ◽  
Neuronal Excitability

Comprehensive analysis of the ascidian genome reveals novel insights into the molecular evolution of ion channel genes

2005 ◽  
Vol 22 (3) ◽  
pp. 269-282 ◽  
Author(s):  
Yasushi Okamura ◽  
Atsuo Nishino ◽  
Yoshimichi Murata ◽  
Koichi Nakajo ◽  
Hirohide Iwasaki ◽  
...  
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Physical Environment ◽  
Chloride Channels ◽  
Transient Receptor Potential ◽  
Neuronal Excitability ◽  
Receptor Potential ◽  
Crown Group ◽  
Homeostatic Control ◽  
Neuronal Signaling

Ion fluxes through membrane ion channels play crucial roles both in neuronal signaling and the homeostatic control of body electrolytes. Despite our knowledge about the respective ion channels, just how diversification of ion channel genes underlies adaptation of animals to the physical environment remains unknown. Here we systematically survey up to 160 putative ion channel genes in the genome of Ciona intestinalis and compare them with corresponding gene sets from the genomes of the nematode Chaenorhabditis elegans, the fruit fly Drosophila melanogaster, and the more closely related genomes of vertebrates. Ciona has a set of so-called “prototype” genes for ion channels regulating neuronal excitability, or for neurotransmitter receptors, suggesting that genes responsible for neuronal signaling in mammals appear to have diversified mainly via gene duplications of the more restricted members of ancestral genomes before the ascidian/vertebrate divergence. Most genes responsible for modulation of neuronal excitability and pain sensation are absent from the ascidian genome, suggesting that these genes arose after the divergence of urochordates. In contrast, the divergent genes encoding connexins, transient receptor potential-related channels and chloride channels, channels involved rather in homeostatic control, indicate gene duplication events unique to the ascidian lineage. Because several invertebrate-unique channel genes exist in Ciona genome, the crown group of extant vertebrates not only acquired novel channel genes via gene/genome duplications but also discarded some ancient genes that have persisted in invertebrates. Such genome-wide information of ion channel genes in basal chordates enables us to begin correlating the innovation and remodeling of genes with the adaptation of more recent chordates to their physical environment.

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