Voltage-activated calcium channels involved in veratridine-evoked [3H]dopamine release in rat striatal slices

Dobrev, Dobromir; Milde, A. S.; Andreas, K; Ravens, Ursula

doi:10.1016/s0028-3908(98)00103-8

Cited by 14 publications

(18 citation statements)

References 39 publications

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“…The DHP-sensitive current component displayed a marked time dependent inactivation with Ti = 56 ± 6 and T2 = 726 ± 88 ms, respectively (n = 7; Fig. As the current sensitive to w-conotoxin MVIIC could be either P-or Q-type, the funnel web spider toxin w-agatoxin TK, a potent and selective P-type current blocker (Teramoto et al, 1993;Dobrev et al, 1998), was used next. The N-type specific Ca 2+ current blocker w-conotoxin GVIA (1 (xM) irreversibly inhibited 27 ± 8 % (n = 4; Fig.…”

Section: Identification Of Hva Ca 2+ Current Components In Dlgn Relaymentioning

confidence: 99%

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Meuth¹,

Budde²,

Pape³

2001

THL

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Ca 2+ -dependent inactivation of Ca 2+ channels represents a feedback mechanism to limit the influx of Ca 2+ into cells. Since large Ca 2+ transients are present in thalamocortical relay neurons and Ca 2+ -dependent mechanisms play a pivotal role for thalamic physiology, the existence of this inactivation mechanism and the involvement of different Ca 2+ channel subtypes was investigated. The use of subtype-specific antibodies revealed the expression of a l A -a l E channel proteins on the cell body and proximal dendrites of acutely isolated cells from the rat dorsolateral geniculate nucleus (dLGN). In addition, subtype-specific channel blocking agents were used in whole cell patch clamp experiments: nifedipine (1-5 jxM; L-type) blocked 35 ± 3%, co-conotoxin GVIA (1 |xM; N-type) blocked 27 ± 8%, and w-conotoxin MVIIC (4 |xM; P/Q-type) blocked 33 ± 5% of the total HVA Ca 2+ current. The blocker-resistant current constituted about 12 ± 3% of the total Ca 2+ current. The degree of Ca 2+ current inactivation was assessed by using a two-pulse protocol. Under control conditions the post-pulse I/V was U-shaped with 35 ± 4% of the current undergoing inactivation. Inclusion of BAPTA to the internal pipette solution reduced the degree of inactivation to 15 ± 1%. When L-and P/Q-type current was blocked, the degree of inactivation was lowered to 20 ± 2 and 27 ± 3%, respectively. In the presence of w-agatoxin TK (35 ± 6%) and w-conotoxin GVIA (32 ± 1%) there was no change in inactivation. These data suggest that Ca 2+ -dependent inactivation is involved in the fine tuning of Ca 2+ entry into relay neurons mediated by L-and Q-type channels locally operated by Ca 2+ beneath the plasma membrane.

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Section: Identification Of Hva Ca 2+ Current Components In Dlgn Relaymentioning

confidence: 99%

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Meuth¹,

Budde²,

Pape³

2001

THL

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“…We tentatively attribute this effect to the long estabished membrane stabilizing effect of Ca 2+ [18], while at lower [Ca 2+ ] o , the established labilizing effect of veratridine may cause channel activation [7,42]. Similarly, in chromaffin cells, high [Ca 2+ ] o entails reduced veratridine-induced [Ca 2+ ] i increase [31] and catecholamine release [10,12]. Alternatively, other membrane stabilizing agents, like quinidine, can abolish veratridine effects [50].…”

Section: Discussionmentioning

confidence: 89%

“…Just like in some other cell types [2,8,21,42], including neuronal systems [1,7,12,13,17,31,51], veratridine induces exocytosis in Paramecium cells [15,24,29,36]. Depending on the cell type analyzed, mechanisms involved in veratridine activation may range from depolarization by activation of Na channels to Na o + -independent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…[26]. Since [Ca 2+ ] i can decrease with time, when Ca o 2+ is removed [12], the fast Ca 2+ chelator BAPTA (1 mM final concentration) was eventually added to the veratridine solution. In some controls, vehicle only was applied.…”

Section: Cell Culturesmentioning

confidence: 99%

“…Veratridine is frequently assumed to act from outside the cell, but it may also become active from inside the cell [19,22], whereby it would have to penetrate the cell membrane [8,22]. Activation of Na channels [1,7,22,52], or possibly also of Na + /Ca 2+ exchangers [52] or of Ca channels [12,51] may then ensue.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Veratridine-Mediated Ca 2+ Dynamics and Exocytosis in Paramecium Cells

Blanchard

Klauke

Zitzmann

et al. 1999

Journal of Membrane Biology

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Thapsigargin‐induced Ca²⁺ increase inhibits TGFβ1‐mediated Smad2 transcriptional responses via Ca²⁺/calmodulin‐dependent protein kinase II

Ming¹,

Manzini²,

Le³

et al. 2010

J of Cellular Biochemistry

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Transforming growth factor β (TGFβ) signalling plays important roles in a variety of tissues and cell types. Impaired TGFβ signalling contributes to several pathologies, including cancer, fibrosis as well as neurodegenerative diseases. TGFβ receptor type I-mediated phosphorylation of Smad2, the formation of the Smad2-Smad4 complex and translocation to the nucleus are critical steps of the TGFβ signalling pathway. Here, we demonstrate that thapsigargin-mediated increase of intracellular Ca(2+) concentrations inhibited TGFβ1-induced Smad2 transcriptional activity in the oligodendroglial cell line OLI-neu. We provide evidence that thapsigargin treatment dramatically reduced the nuclear translocation of Smad2 after TGFβ1 treatment but had no effect on its phosphorylation at Ser465/467. Moreover, using Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitors and a constitutively active CaMKII mutant, we provide evidence that the observed inhibition of TGFβ signalling in OLI-neu cells was strongly dependent on Ca(2+)-mediated CaMKII activation. In summary, this study clearly shows that the TGFβ1-induced Smad2 nuclear translocation is negatively regulated by intracellular Ca(2+) in OLI-neu cells and that increased intracellular Ca(2+) concentrations block Smad2-mediated transcription of TGFβ target genes. These results underline the importance of intracellular Ca(2+) for the regulation of TGFβ signalling.

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Voltage-activated calcium channels involved in veratridine-evoked [3H]dopamine release in rat striatal slices

Cited by 14 publications

References 39 publications

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Veratridine-Mediated Ca 2+ Dynamics and Exocytosis in Paramecium Cells

Thapsigargin‐induced Ca²⁺ increase inhibits TGFβ1‐mediated Smad2 transcriptional responses via Ca²⁺/calmodulin‐dependent protein kinase II

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Voltage-activated calcium channels involved in veratridine-evoked [3H]dopamine release in rat striatal slices

Cited by 14 publications

References 39 publications

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Differential control of high-voltage activated Ca 2+ current components by a Ca 2+ -dependent inactivation mechanism in thalamic relay neurons

Veratridine-Mediated Ca 2+ Dynamics and Exocytosis in Paramecium Cells

Thapsigargin‐induced Ca2+ increase inhibits TGFβ1‐mediated Smad2 transcriptional responses via Ca2+/calmodulin‐dependent protein kinase II

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Thapsigargin‐induced Ca²⁺ increase inhibits TGFβ1‐mediated Smad2 transcriptional responses via Ca²⁺/calmodulin‐dependent protein kinase II