Distinct effects of ω-toxins and various groups of Ca2+-entry inhibitors on nicotinic acetylcholine receptor and Ca2+ channels of chromaffin cells

Villarroya, Mércedes; Fuente, María-Teresa de la; López, Manuela G.; Gandı́a, Luis; Garcı́a, Antonio G.

doi:10.1016/s0014-2999(96)00902-8

Cited by 30 publications

(17 citation statements)

References 29 publications

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“…This relative contribution of each Ca 2+ channel subtype to the [Ca 2+ ] i increase induced by 38 m M K + differs from previous data concerning the relative densities of Ca 2+ channel subtypes in bovine chromaffin cells. Thus, using 45 Ca 2+ uptake in cells stimulated with 70 m M K + (Villarroya et al., 1997) or depolarizing pulses from ‐80 mV to 0 mV in voltage‐clamped cells (Albillos et al, 1996), we came to the conclusion that L channels account for 20%, N channels for 30%, and P/Q channels for 50% of the total population of Ca 2+ channels present in bovine chromaffin cells. In neurons and chromaffin cells, L‐type channels are activated at more negative potentials than non‐L‐type channels (Carbone et al, 1990; Albillos et al, 1994); also, in chromaffin cells N and P/Q subtypes are more prone than the L subtype to inactivation at depolarizing voltages (Villarroya et al, 1999).…”

Section: High K+ Enhances Mrna and Protein Levels Of Snap‐25mentioning

confidence: 99%

Multiple Calcium Pathways Induce the Expression of SNAP‐25 Protein in Chromaffin Cells

Garcı́a-Palomero¹,

Montiel²,

Herrero³

et al. 2000

Journal of Neurochemistry

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Incubation of bovine adrenal chromaffin cells in high K ϩ (38 mM) during 24 -48 h enhanced 2.5 to five times the expression of SNAP-25 protein and mRNA, respectively. This increase was reduced 86% by furnidipine (an L-type Ca 2ϩ channel blocker) but was unaffected by either -conotoxin GVIA (an N-type Ca 2ϩ channel blocker) or -agatoxin IVA (a P/Q-type Ca 2ϩ channel blocker). Combined blockade of N and P/Q channels with -conotoxin MVIIC did, however, block by 76% the protein expression. The inhibitory effects of furnidipine were partially reversed when the external Ca 2ϩ concentration was raised from 1.6 to 5 mM. These findings, together with the fact that nicotinic receptor activation or Ca 2ϩ release from internal stores also enhanced SNAP-25 protein expression, suggest that an increment of cytosolic Ca 2ϩ concentration ([Ca 2ϩ ] i ), rather than its source or Ca 2ϩ entry pathway, is the critical signal to induce the protein expression. The greater coupling between L-type Ca 2ϩ channels and protein expression might be due to two facts: (a) L channels contributed 50% to the global [Ca 2ϩ ] i rise induced by 38 mM K ϩ in indo-1-loaded chromaffin cells and (b) L channels undergo less inactivation than N or P/Q channels on sustained stimulation of these cells.

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Section: High K+ Enhances Mrna and Protein Levels Of Snap‐25mentioning

confidence: 99%

Multiple Calcium Pathways Induce the Expression of SNAP‐25 Protein in Chromaffin Cells

Garcı́a-Palomero¹,

Montiel²,

Herrero³

et al. 2000

Journal of Neurochemistry

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“…The VOCCs present in bovine chromaffin cells iclude the L, N and P/Q subtypes (Garcia et al, 2006). Each VOCC subtype has been found to contribute to 45 Ca 2+ entry (Ballesta et al, 1989;Lopez et al, 1994;Villarroya et al, 1997) and catecholamine release (Lopez et al, 1994;Lara et al, 1998). However, N and P/Q channels are inactivated at depolarizing voltages, in contrast to the L-subtype (Villarroya et al, 1999), and this inactivation blocks Ca 2+ entry and catecholamine release (Artalejo et al, 1986;Michelena et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Calcium signalling mediated through α7 and non‐α7 nAChR stimulation is differentially regulated in bovine chromaffin cells to induce catecholamine release

Barrio

Egea

León

et al. 2010

British J Pharmacology

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BACKGROUND AND PURPOSE Ca2+ signalling and exocytosis mediated by nicotinic receptor (nAChR) subtypes, especially the a7 nAChR, in bovine chromaffin cells are still matters of debate. EXPERIMENTAL APPROACHWe have used chromaffin cell cultures loaded with Fluo-4 or transfected with aequorins directed to the cytosol or mitochondria, several nAChR agonists (nicotine, 5-iodo-A-85380, PNU282987 and choline), and the a7 nAChR allosteric modulator PNU120596. KEY RESULTS Minimal [Ca 2+]c transients, induced by low concentrations of selective a7 nAChR agonists and nicotine, were markedly increased by the a7 nAChR allosteric modulator PNU120596. These potentiated responses were completely blocked by the a7 nAChR antagonist a-bungarotoxin (a7-modulated-response). Conversely, high concentrations of the a7 nAChR agonists, nicotine or 5-iodo-A-85380 induced larger [Ca 2+ ]c transients, that were blocked by mecamylamine but were unaffected by a-bungarotoxin (non-a7 response). [Ca 2+ ]c increases mediated by a7 nAChR were related to Ca 2+ entry through non-L-type Ca 2+ channels, whereas non-a7 nAChR-mediated signals were related to L-type Ca 2+ channels; Ca [Ca 2+ ]c and catecholamine release mediated by a7 nAChRs required an allosteric modulator and low doses of the agonist. At higher agonist concentrations, the a7 nAChR response was lost and the non-a7 nAChRs were activated. Catecholamine release might therefore be regulated by different nAChR subtypes, depending on agonist concentrations and the presence of allosteric modulators of a7 nAChRs. [Ca 2+ ]c, cytosolic concentration of calcium; BGT, a-bungarotoxin; DMEM, Dulbecco's modified Eagle's medium; ER, endoplasmic reticulum; nAChR, nicotinic acetylcholine receptor; VOCC, voltage operated calcium channel BJP British Journal of Pharmacology CONCLUSIONS AND IMPLICATIONS Abbreviations

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“…It suggests that LESM and nitrendipine interact with the same Ca 2+ channels subtype. However, it had been reported that various dihydropyridines Ca 2+ channel blockers including nitrendipine blocked both L-type Ca 2+ channels and neural nicotinic receptors (Lopez et al, 1993;Villarroya et al, 1997). Since nitrendipine may affect both the L-type calcium channel and the nicotinic receptor, we further studied the effect of Hex on CA secretion induced by LESM.…”

Section: Discussionmentioning

confidence: 99%

“…Since it had been reported that various dihydropyridines Ca 2+ channel blockers including nitrendipine blocked both L-type Ca 2+ channels and neural nicotinic receptors (Lopez et al, 1993;Villarroya et al, 1997). We examined the effects of hexamethonium (Hex), an inhibitor of nAChR (Vainio et al, 1998), on basal CA secretion induced by 50 g/ml LESM.…”

Section: Stimulatory Modes Of Lesm On Basal Ca Secretion In Cultured mentioning

confidence: 99%

Dual effects of lipophilic extract of Salvia miltiorrhiza (Danshen) on catecholamine secretion in cultured bovine adrenal medullary cells

Mao¹,

Zhang²,

Wang³

et al. 2009

Journal of Ethnopharmacology

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Distinct effects of ω-toxins and various groups of Ca2+-entry inhibitors on nicotinic acetylcholine receptor and Ca2+ channels of chromaffin cells

Cited by 30 publications

References 29 publications

Multiple Calcium Pathways Induce the Expression of SNAP‐25 Protein in Chromaffin Cells

Multiple Calcium Pathways Induce the Expression of SNAP‐25 Protein in Chromaffin Cells

Calcium signalling mediated through α7 and non‐α7 nAChR stimulation is differentially regulated in bovine chromaffin cells to induce catecholamine release

Dual effects of lipophilic extract of Salvia miltiorrhiza (Danshen) on catecholamine secretion in cultured bovine adrenal medullary cells

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