Voltage‐ and Ca2+‐activated potassium channels in Ca2+ store control Ca2+ release

Yamashita, Masayuki; Sugioka, Miho; Ogawa, Yoichi

doi:10.1111/j.1742-4658.2006.05365.x

Cited by 32 publications

(66 citation statements)

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Section: 'Luminal Potential' Modelmentioning

confidence: 99%

“…In fact, voltage-and Ca 2+ -activated potassium (BK-type) channels are present in the nuclear envelope or perinuclear ER [32,33]. The store BK channel is activated by positive shifts in the luminal potential and luminal Ca 2+ increases [32,33]. From these properties of the store BK channel and the dynamics of the membrane potential of Ca 2+ store, 'luminal potential' model has been proposed to account for 'quantal' Ca 2+ release [32].…”

Section: 'Luminal Potential' Modelmentioning

confidence: 99%

“…The store BK channel is activated by positive shifts in the luminal potential and luminal Ca 2+ increases [32,33]. From these properties of the store BK channel and the dynamics of the membrane potential of Ca 2+ store, 'luminal potential' model has been proposed to account for 'quantal' Ca 2+ release [32]. In this model, the store BK channel is closed by a Ca 2+ release-induced negative shift in the luminal potential and a decrease in the luminal Ca 2+ concentration.…”

Section: 'Luminal Potential' Modelmentioning

confidence: 99%

“…The resultant depolarization would resume Ca 2+ release. In fact, the luminal potential oscillates bistably by 45 mV in amplitude [32].…”

Section: Ca 2+ Oscillation By 'Quantal' Ca 2+ Releasementioning

confidence: 99%

“…2, right). In fact, the luminal potential oscillation is highly synchronized at the depolarization phase [32]. This may be an example of 'pulse-coupled' oscillators [50].…”

Section: Synchronization Of Oscillatory Ca 2+ Releasementioning

confidence: 99%

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‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization

Yamashita

2006

FEBS Letters

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Ca 2+ release from intracellular Ca 2+ stores, a pivotal event in Ca 2+ signaling, is a 'quantal' process; it terminates after a rapid release of a fraction of stored Ca 2+ . To explain the 'quantal' nature, 'all-or-none' model and 'steady-state' model were proposed. This article shortly reviews these hypotheses and considers a recently proposed mechanism, 'luminal potential ' model, in The release of Ca 2+ from intracellular Ca 2+ stores shows complex kinetic behavior. By examining the kinetics of hormone-mediated 45 Ca 2+ efflux from pre-loaded stores, Muallem et al. [1] found that the Ca 2+ release is a 'quantal' rather than a continuous process; it consists of a rapid release of a fraction of stored Ca 2+ followed by no or a much slower efflux of Ca 2+ . This transient and partial release behavior has been termed 'quantal' Ca 2+ release [1].The 'quantal' release of Ca 2+ requires a mechanism for the attenuation of Ca 2+ efflux, such as inactivation of inositol 1,4,5-trisphosphate (InsP 3 ) receptor channels [2]. However, many studies have provided evidence for the lack of inactivation or desensitization of InsP 3 receptor channels [3][4][5][6][7][8][9]. Alternatively, the efflux of Ca 2+ may be compensated for by reuptake of Ca 2+ after a rapid release of Ca 2+ , as the activity of store Ca 2+ pumps is accelerated by a decrease in the concentration of Ca 2+ in the lumen of the Ca 2+ store [10]. However, this explanation was also unlikely because the transient Ca 2+ release occurs in the absence of Ca 2+ reuptake [3,4,8,9,[11][12][13].Another feature of 'quantal' Ca 2+ release is that the amount of Ca 2+ released depends on the dose of agonist or InsP 3 [1,3,4,6,8,9], or caffeine for ryanodine-sensitive Ca 2+ stores [14,15]. Meyer and Stryer [3] suggested that such dose dependent Ca 2+ release acts as an 'increment detector' in response to stepwise increases in stimulus intensity. To explain the kinetics and the dose dependence of 'quantal' Ca 2+ release, the following two hypotheses were proposed. 'All-or-none' model versus 'steady-state' modelMuallem et al.[1] first postulated that Ca 2+ ions are released from Ca 2+ stores in an all-or-none fashion ('all-or-none' model). Then Irvine [16] proposed another model, in which the sensitivity of InsP 3 receptor to InsP 3 is regulated by the luminal Ca 2+ concentration ('steady-state' model). Since these two models were proposed, numerous studies attempted to support or deny either of the two hypotheses. Missiaen et al.[17] and Bootman [18] extensively reviewed and discussed these hypotheses. The following is a short review of the two models including recent studies. All-or-none modelMuallem et al.[1] have supposed that intracellular Ca 2+ stores are compartmentalized and a submaximal dose of agonist or InsP 3 discharges all the Ca 2+ content in a fraction of the compartmentalized Ca 2+ stores. It is also assumed that the compartments of Ca 2+ store differ in the sensitivity to InsP 3 . According to this model, all the stored Ca 2+ ions are released fro...

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Section: 'Luminal Potential' Modelmentioning

confidence: 99%

Section: 'Luminal Potential' Modelmentioning

confidence: 99%

Section: 'Luminal Potential' Modelmentioning

confidence: 99%

“…The resultant depolarization would resume Ca 2+ release. In fact, the luminal potential oscillates bistably by 45 mV in amplitude [32].…”

Section: Ca 2+ Oscillation By 'Quantal' Ca 2+ Releasementioning

confidence: 99%

“…2, right). In fact, the luminal potential oscillation is highly synchronized at the depolarization phase [32]. This may be an example of 'pulse-coupled' oscillators [50].…”

Section: Synchronization Of Oscillatory Ca 2+ Releasementioning

confidence: 99%

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‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization

Yamashita

2006

FEBS Letters

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Ion channels of the nuclear membrane of hippocampal neurons

Fedorenko

Marchenko

2014

Hippocampus

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Rise in Ca(2+) concentration in the nucleus affects gene transcription and has been implicated in neuroprotection, transcription-dependent neuronal plasticity, and pain modulation, but the mechanism of regulation of nuclear Ca(2+) remains poorly understood. The nuclear envelope is a part of the endoplasmic reticulum and may be one of the sources of nuclear Ca(2+) . Here, we studied ion channels in the nuclear membrane of hippocampal neurons using the patch-clamp technique. We have found that the nuclear membrane of CA1 pyramidal and dentate gyrus granule (DG), but not CA3 pyramidal neurons, was enriched in functional inositol 1,4,5-trisphosphate receptors/Ca(2+) -release channels (IP3 Rs) localized mainly in the inner nuclear membrane. A single nuclear ryanodine receptor (RyR) has been detected only in DG granule neurons. Nuclei of the hippocampal neurons also expressed a variety of spontaneously active cation and anion channels specific for each type of neuron. In particular, large-conductance ion channels selective for monovalent cations (LCC) were coexpressed with IP3 Rs. These data suggest that: (1) the nuclear membranes of hippocampal neurons contain distinct sets of ion channels, which are specific for each type of neuron; (2) IP3 Rs, but not RyRs are targeted to the inner nuclear membrane of CA1 pyramidal and DG granule, but they were not found in the nuclear membranes of CA3 pyramidal neurons; (3) the nuclear envelope of these neurons is specialized to release Ca(2+) into the nucleoplasm which may amplify Ca(2+) signals entering the nucleus from the cytoplasm or generate Ca(2+) transients on its own; (4) LCC channels are an integral part the of Ca(2+) -releasing machinery providing a route for counterflow of К(+) and thereby facilitating Ca(2+) movement in and out of the Ca(2+) store.

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Identification and quantification of full‐length BK channel variants in the developing mouse cochlea

Sakai

Harvey

Sokolowski

2011

J of Neuroscience Research

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Maxi K+ (BK) channel diversity is attributed to alternative splicing in the kcnma1 gene. The resultant variants manifest themselves in different cell types, tissues and functions such as excitation, metabolism, and signaling. Immuno-electron microscopy revealed immunogold particle labeling of BK in apical and basal regions of inner and outer hair cells, respectively. Additional labeling occurs in Deiters’ cells and the inner mitochondrial membrane. Identification of full-length sequences reveals 27 BK variants from embryonic and postnatal mouse inner ear, per classification by tail motif, VYR, DEC, and ERL, and by exon usage. Three predicted start codons are found encoding MAN, MSS, and MDA, of which MDA shows the greatest expression through all stages in development, whereas MAN is undetectable. Complex splice sites occur between exons 9 and 10, and 21 and 23. Spliced-in/out exons between 8 and 10 reveal a short fragment composed of exons 8+10, detectable on postnatal-day (PD) 14 and PD30, and a longer fragment composed of exons 8+9+10 that upregulates on embryonic-day (ED) 14. Spliced-in exons 22 or 23 are expressed on ED14 but decrease over time; however, exon 22 increases again on PD34. Using tail specific primers, qRT-PCR from ED14, PD4, 14, and 30, show that BK-VYR and -ERL dominate expression on ED14, whereas DEC dominates after birth in all cochlear regions. The localization of BK and the changes in expression of its exons and tail types, by alternative splicing during development, may contribute to cochlear organization, acquisition of hearing, and intracellular signaling.

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Voltage‐ and Ca²⁺‐activated potassium channels in Ca²⁺ store control Ca²⁺ release

Cited by 32 publications

References 50 publications

‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization

‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization

Ion channels of the nuclear membrane of hippocampal neurons

Identification and quantification of full‐length BK channel variants in the developing mouse cochlea

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Voltage‐ and Ca2+‐activated potassium channels in Ca2+ store control Ca2+ release

Cited by 32 publications

References 50 publications

‘Quantal’ Ca2+ release reassessed – a clue to oscillation and synchronization

‘Quantal’ Ca2+ release reassessed – a clue to oscillation and synchronization

Ion channels of the nuclear membrane of hippocampal neurons

Identification and quantification of full‐length BK channel variants in the developing mouse cochlea

Contact Info

Product

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About

Voltage‐ and Ca²⁺‐activated potassium channels in Ca²⁺ store control Ca²⁺ release

‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization

‘Quantal’ Ca²⁺ release reassessed – a clue to oscillation and synchronization