Regulation of CaV3.1 Channels by Glucocorticoids

Avila, Traudy; Hernández-Hernández, Óscar; Almanza, Angélica; León, Mario Bermúdez de; Urbán, Mercedes; Soto, Enrique; Cisneros, Bulmaro; Felix, Ricardo

doi:10.1007/s10571-009-9422-2

Cited by 5 publications

(3 citation statements)

References 43 publications

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“…A subset of these antibodies (Ca V 1.2, Ca V 2.1, Ca V 2.2, Ca V 2.3) have also been examined in cochlear sections (Lopez et al, 2003). Anti-Ca v 3.3 antibody, directed against amino acids 1053–1067 in the intracellular loop between domain II and III, has also been characterized by Western blot analysis of transfected HEK 293 cells stably expressing Ca v 3.3 protein, which showed a single band at ~200 kD (Avila et al, 2009; Zhang et al, 2006) that was is absent in native HEK 293 cells. Anti-Ca V 1.3 antibody, obtained from NeuroMab (UC Davis/NIH), showed specific localization to ~250 kD with Western blot analysis.…”

Section: Methodsmentioning

confidence: 99%

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

et al. 2011

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As with other elements of the peripheral auditory system, spiral ganglion neurons display specializations that vary as a function of location along the tonotopic axis. Previous work has shown that voltage-gated K+ channels and synaptic proteins show graded changes in their density that confers rapid responsiveness to neurons in the high frequency, basal region of the cochlea and slower, more maintained responsiveness to neurons in the low frequency, apical region of the cochlea. In order to understand how voltage-gated calcium channels (VGCCs) may contribute to these diverse phenotypes, we identified the VGCC α-subunits expressed in the ganglion, investigated aspects of Ca2+-dependent neuronal firing patterns, and mapped the intracellular and intercellular distributions of seven VGCC α-subunits in the spiral ganglion in vitro. Initial experiments with qRT-PCR showed that eight of the ten known VGCC α-subunits were expressed in the ganglion and electrophysiological analysis revealed firing patterns that were consistent with the presence of both LVA and HVA Ca2+ channels. Moreover, we were able to study seven of the α-subunits with immunocytochemistry, and we found that all were present in spiral ganglion neurons, and that three of them were neuron-specific (CaV1.3, CaV2.2, and CaV3.3). Further characterization of neuron-specific α-subunits showed that CaV1.3 and CaV3.3 were tonotopically-distributed, whereas CaV2.2 was uniformly distributed in apical and basal neurons. Multiple VGCC α-subunits were also immunolocalized to Schwann cells, having distinct intracellular localizations, and, significantly, appearing to distinguish putative compact0 (CaV2.3, CaV3.1) from loose (CaV1.2) myelin. Electrophysiological evaluation of spiral ganglion neurons in the presence of TEA revealed Ca2+ plateau potentials with slopes that varied proportionately with the cochlear region from which neurons were isolated. Because afterhyperpolarizations were minimal or absent under these conditions, we hypothesize that differential density and/or kinetics of one or more of the VGCC α-subunits could account for observed tonotopic differences. These experiments have set the stage for defining the clear multiplicity of functional control in neurons and Schwann cells of the spiral ganglion.

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Section: Methodsmentioning

confidence: 99%

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

et al. 2011

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“…Reverse transcription (RT) was performed using iScript cDNA Synthesis kit (Bio-Rad), followed by PCR and agarose gel analysis. The primers used for the PCR were reported previously (Latour et al, 2003;Li and Zhang, 2009;Avila et al, 2009) and are listed in Table 1.…”

Section: Rt-pcrmentioning

confidence: 99%

Spontaneous Local Calcium Transients Regulate Oligodendrocyte Development in Culture through Store-Operated Ca²⁺Entry and Release

Rui

Pollitt

Myers

et al. 2020

eNeuro

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Oligodendrocytes (OLs) insulate axonal fibers for fast conduction of nerve impulses by wrapping axons of the CNS with compact myelin membranes. Differentiating OLs undergo drastic chances in cell morphology. Bipolar oligodendroglial precursor cells (OPCs) transform into highly ramified multipolar OLs, which then expand myelin membranes that enwrap axons. While significant progress has been made in understanding the molecular and genetic mechanisms underlying CNS myelination and its disruption in diseases, the cellular mechanisms that regulate OL differentiation are not fully understood. Here, we report that developing rat OLs in culture exhibit spontaneous Ca 21 local transients (sCaLTs) in their process arbors in the absence of neurons. Importantly, we find that the frequency of sCaLTs markedly increases as OLs undergo extensive process outgrowth and branching. We further show that sCaLTs are primarily generated through a combination of Ca 21 influx through store-operated Ca 21 entry (SOCE) and Ca 21 release from internal Ca 21 stores. Inhibition of sCaLTs impairs the elaboration and branching of OL processes, as well as substantially reduces the formation of large myelin sheets in culture. Together, our findings identify an important role for spontaneous local Ca 21 signaling in OL development.

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“…This form of regulation is perhaps in lieu of the apparent lack of association of T‐types with accessory subunits such as the β , α 2 δ , and γ of HVA channels (although see Refs 205, 142, and 206), allowing for the up‐ or downregulation of surface‐expressed channels without a requirement for posttranslational, multimeric subunit assembly. Various growth factors,207,208 hormones,147,209–211 and transcription factors147,212,213 have been implicated in T‐type channel transcription. The human Ca v 3.1 gene is under the control of two different promoters, which are differentially expressed during neuronal differentiation 88.…”

Section: Modulation Of Functionmentioning

confidence: 99%

Ca_v3 T‐type calcium channels

Senatore

Zhorov

Spafford

2012

WIREs Membr Transp Signal

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T-type channels are unique among the voltage-gated calcium channels in their fast kinetics and low voltages of activation and inactivation, the latter two features allowing them to operate at voltages near the resting membrane potential of most neurons. T-type channels can therefore be recruited by subthreshold depolarizations, and hyperpolarizations that remove inactivation. As such, T-type channels can significantly influence how and when cells reach action potential threshold, and thus are critical regulators of excitability. T-type channels are also significantly conserved within the animal kingdom, present even in animals lacking muscles and nerves, suggesting that they evolved before or very early on during the emergence of neuronal and neuromuscular synapses. Physiologically, T-type channels are involved in multiple processes, and their contributions range from purely electrogenic roles to the activation of calcium-sensitive ion channels, signaling pathways, and other macromolecular complexes. Unfortunately, it has been difficult to prove sufficiency and necessity of T-type channels in many of these processes, in part due to inconsistencies in their suspected contributions. INTRODUCTION Voltage-gated calcium channels of the Ca v 3 family, or T-type calcium channels, likely evolved in animals either before or during the very early stages of nervous system evolution, and were subsequently adapted for electrical excitability and calcium signaling in different cell types including neurons, muscle and secretory cells. Although intensively studied, the lack of specific blockers has made it difficult to ascribe T-type channels with specific functions. Recent advances in imaging and electrophysiological techniques, along with the discovery of novel-blocking compounds and the * Correspondence to: spafford@uwaterloo.ca 1 Department of Biology, University of Waterloo, Waterloo, Ontario, Canada 2 Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada development of molecular and biological tools, have paved the way for accelerated discovery. A clearer picture is emerging, where T-type channel functions are ascribed to particular Ca v 3 isotype(s), and which vary depending on the configuration of calcium-sensitive factors (i.e., calcium-sensitive signaling pathways and ionic conductances) present in cells, and also on the electrical properties of cells as determined by other ion channels, receptors, and pumps. HISTORY OF T-TYPE CURRENT ISOLATIONT-type calcium currents were first isolated in the 1970s by Susumu Hagiwara in invertebrate starfish eggs using two-electrode voltage clamp.1 'Channel I' currents were evoked by small depolarizations, (Figure 1(a)). Subsequent voltage clamp studies also identified channel I currents in vertebrate preparations, including guinea-pig inferior olivary 2 and thalamic neurons 3 and chick sensory neurons. 4 The term 'T-type channel' was coined on the basis of the transient (rapid) kinetics and tiny unitary conductance of channel I type cur...

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Regulation of CaV3.1 Channels by Glucocorticoids

Cited by 5 publications

References 43 publications

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

Spontaneous Local Calcium Transients Regulate Oligodendrocyte Development in Culture through Store-Operated Ca²⁺Entry and Release

Ca_v3 T‐type calcium channels

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Regulation of CaV3.1 Channels by Glucocorticoids

Cited by 5 publications

References 43 publications

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion

Spontaneous Local Calcium Transients Regulate Oligodendrocyte Development in Culture through Store-Operated Ca2+Entry and Release

Cav3 T‐type calcium channels

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Product

Resources

About

Spontaneous Local Calcium Transients Regulate Oligodendrocyte Development in Culture through Store-Operated Ca²⁺Entry and Release

Ca_v3 T‐type calcium channels