Molecular physiology and modulation of somatodendritic A-type potassium channels

Jerng, Henry H.; Pfaffinger, Paul J.; Covarrubias, Manuel

doi:10.1016/j.mcn.2004.06.011

Cited by 273 publications

(433 citation statements)

References 232 publications

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“…Thus, the diversity of complex formation between KChIPs and their target molecules (see below) may be further increased by the oligomerization of KChIPs with a number of closely and more distantly related proteins [42]. KChIPs have three main types of specific target molecules, and three corresponding functions are attributed to the KChIPs: Some of them have been shown to interact with presenilins to control Ca 2+ signaling and apoptosis (Figure 1B), and some have been shown to interact with DNA to control gene expression (Figure 1C), but all KChIPs interact with Kv4 channels (Figure 1D) to form I SA and control neuronal excitation [5,12]. Moreover, due to the expression of KChIP2 as a critical component of the Kv4 channel-mediated I to in cardiomyocytes [8,43,44], it is obvious that KChIPs also play an important role in non-neuronal excitation.…”

Section: Ca2+ Binding Properties and Associated Conformational Changementioning

confidence: 99%

“…the molecular substrate of transient potassium currents in heart and brain [5,8,12]. Heterologous coexpression of KChIPs (except for the KChIP4a splice variant, see below) leads to an increase in surface expression of Kv4 channels and to a modulation of their inactivation gating, namely, a slowing of the initial phase of macroscopic current decay, an acceleration of the recovery from inactivation and a positive shift of the voltage dependence of steady-state inactivation (Figure 1(e)).…”

Section: Ca2+ Dependence Of Kv4/kchip Complex Formation and Membrane mentioning

confidence: 99%

“…Rather, these authors most specifically searched for interaction partners with a yeast two hybrid bait corresponding to the cytoplasmic N-terminus (180 amino acids) of the Kv4.3 subtype of Kv4 channels. These channels are related to the Shal gene of Drosophila melanogaster [3,4], and mediate both the subthreshold-activating somatodendritic A-type current (I SA ) in neurons [5,6] and the transient outward current (I to ) in cardiomyocytes [7–9]. The search for Kv4 channel auxiliary β-subunits had been driven by the finding that coexpression of a low molecular weight brain mRNA fraction (2 – 4 kb) caused an increase in surface expression and a modification of the biophysical properties of Shal -related A-type (i.e., rapidly inactivating) channels [10,11], and, in fact, heterologous coexpression of the newly identified KChIPs had very similar effects on Kv4 channels [1].…”

Section: Introductionmentioning

confidence: 99%

“…The search for Kv4 channel auxiliary β-subunits had been driven by the finding that coexpression of a low molecular weight brain mRNA fraction (2 – 4 kb) caused an increase in surface expression and a modification of the biophysical properties of Shal -related A-type (i.e., rapidly inactivating) channels [10,11], and, in fact, heterologous coexpression of the newly identified KChIPs had very similar effects on Kv4 channels [1]. It is now widely accepted that KChIPs, together with dipeptidyl aminopeptidase-like proteins (DPPs), are integral components of native A-type potassium channels in neurons and cardiomyocytes [5,8,12,13]. …”

Section: Introductionmentioning

confidence: 99%

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Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors

Bähring

2018

Channels

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Kv channel-interacting proteins (KChIPs) belong to the neuronal calcium sensor (NCS) family of Ca2+-binding EF-hand proteins. KChIPs constitute a group of specific auxiliary β-subunits for Kv4 channels, the molecular substrate of transient potassium currents in both neuronal and non-neuronal tissues. Moreover, KChIPs can interact with presenilins to control ER calcium signaling and apoptosis, and with DNA to control gene transcription. Ca2+ binding via their EF-hands, with the consequence of conformational changes, is well documented for KChIPs. Moreover, the Ca2+ dependence of the presenilin/KChIP complex may be related to Alzheimer’s disease and the Ca2+ dependence of the DNA/KChIP complex to pain sensing. However, only in few cases could the Ca2+ binding to KChIPs be directly linked to the control of excitability in nerve and muscle cells known to express Kv4/KChIP channel complexes. This review summarizes current knowledge about the Ca2+ binding properties of KChIPs and the Ca2+ dependencies of macromolecular complexes containing KChIPs, including those with presenilins, DNA and especially Kv4 channels. The respective physiological or pathophysiolgical roles of Ca2+ binding to KChIPs are discussed.

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Section: Ca2+ Binding Properties and Associated Conformational Changementioning

confidence: 99%

Section: Ca2+ Dependence Of Kv4/kchip Complex Formation and Membrane mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors

Bähring

2018

Channels

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“…I A is observed in the majority of SCN neurons and may play a role in setting the action potential firing frequency in these cells (Bouskila and Dudek, 1995;Huang, 1993;Huang et al, 1993). I A is carried by ion channels composed of α subunits of the Kv4 family (Shal, (Jerng et al, 2004)). In neurons, the observed I A activation and inactivation kinetics require the presence of Kv Channel Interacting Proteins (KChIP).…”

Section: Introductionmentioning

confidence: 99%

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Alvado

Allen

2008

Brain Research

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Identifying the mechanisms that drive suprachiasmatic nucleus (SCN) neurons to fire action potentials with a higher frequency during the day than during the night is an important goal of circadian neurobiology. Selective chemical tools with defined mechanisms of action on specific ion channels are required for successful completion of these studies. The transient K + current (I A ) plays an active role in neuronal action potential firing and may contribute to modulating the circadian firing frequency. Tetraethylammonium (TEA) is frequently used to inhibit delayed rectifier K + currents (I DR ) during electrophysiological recordings of I A . Depolarizing voltage-clamped hamster SCN neurons from a hyperpolarized holding potential activated both I A and I DR . Holding the membrane potential at depolarized values inactivated I A and only the I DR was activated during a voltage step. The identity of I A was confirmed by applying 4-aminopyridine (5 mM), which significantly inhibited I A . Reducing the TEA concentration from 40 mM to 1 mM significantly decreased the I A inactivation time constant (τ inact ) from 9.8 ± 3.0 ms to 4.9 ± 1.2 ms. The changes in I A τ inact were unlikely to be due to a surface charge effect. The I A amplitude was not affected by TEA at any concentration or membrane potential. The isosmotic replacement of NaCl with choline chloride had no effect in I A kinetics demonstrating that the TEA effects were not due to a reduction of extracellular NaCl. We conclude that TEA modulates, in a concentration dependent manner, τ inact but not I A amplitude in hamster SCN neurons. SectionNeurophysiology; Neuropharmacology and other forms of Intercellular Communication

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Self‐Adaptive All‐In‐One Delivery Chip for Rapid Skin Nerves Regeneration by Endogenous Mesenchymal Stem Cells

Peng

Huang

et al. 2020

Adv Funct Materials

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Skin wound therapy aims not only to restore skin protection but also to recover excitation functions through nerve regeneration. During the restoration of skin nerves, the recruitment of endogenous stem cells and promotion of neuronal regeneration on site work stepwise are foundations of in situ regeneration. However, current therapeutic systems usually execute each process separately, leading to limited regeneration and recovery of excitation functions. Herein, a novel self-adaptive all-in-one delivery chip (G:P:Al-Chip) is constructed that combines therapeutic protein release, gene delivery, and electrical conduction in a single microfluidic chip by 3D coaxial printing. G:P:Al-Chip consists of an outer conductive hydrogel shell anchored with chemokine and an inner microchannel filled with enzyme-initiated vector/ plasmid DNAs microcomplexes. G:P:Al-Chip delivers chemokine, functional plasmid DNAs, and promotes electrical conduction with a self-adaptive program that significantly enhances the recruitment of endogenous mesenchymal stem cells and promotes neuronal regeneration. G:P:Al-Chip is shown to enhance nerve regeneration with excitation functions within 23 days. G:P:Al-Chip organizes recruitment and neuronal regeneration cues along with bioelectrical signal in one degradable chip for accelerated skin nerve regeneration.

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Molecular physiology and modulation of somatodendritic A-type potassium channels

Cited by 273 publications

References 232 publications

Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors

Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Self‐Adaptive All‐In‐One Delivery Chip for Rapid Skin Nerves Regeneration by Endogenous Mesenchymal Stem Cells

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