Extracellular ATP regulates exocytosis by inhibiting multiple Ca2+ channel types in bovine chromaffin cells

Ulate, Guido; Scott, Ricardo; González, J. del Boz; Gilabert, J.; Artalejo, Antonio R.

doi:10.1007/s004249900185

Cited by 20 publications

(14 citation statements)

References 28 publications

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“…1996). Ulate et al . (2000) made a study on voltage‐clamped bovine chromaffin cells, measuring I Ca and ΔCm elicited by single 100‐ms depolarizing pulses in 10 m m Ca 2+ .…”

Section: Discussionmentioning

confidence: 99%

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A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice

Aldea

Jun

Shin

et al. 2002

Journal of Neurochemistry

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Simultaneous recordings of inward whole-cell Ca 2+ channel currents (I Ca ) and increments of capacitance as an indication of exocytosis (DCm), were performed in voltage-clamped single adrenal chromaffin cells from wild-type and a 1A subunit deficient mice, using the perforated-patch configuration of the patch-clamp technique. Using protocol #1 (one single Ca 2+ channel blocker per cell), to dissect the components of I Ca , L channels contributed 43%, N channels 35% and P/Q channels 30% to the total I Ca of wild-type cells. Using protocol #2 (cumulative sequential addition of 3 lM nifedipine, 1 lM x-conotoxin GVIA, and 1 lM x-agatoxin IVA), L, N and P/Q channels contributed 40%, 34% and 14%, respectively, to I Ca ; an R component of around 11% remained. In wild-type mice the changes of DCm paralleled those of I Ca . In a 1A deficient mice the L component of I Ca rose to 53% while the P/Q disappeared; the N and R components were similar. In these mice, DCm associated to N and R channels did not vary; however, the P/Q component was abolished while the L component increased by 20%. In conclusion, exocytosis was proportional to the relative density of each Ca 2+ channel subtype, L, N, P/Q, R. Ablation of the a 1A gene led to a loss of P/Q channel current and to a compensatory increase of L channel-associated secretion; however, this compensation was not sufficient to maintain the overall exocytotic response, that was diminished by 35% in a 1A -deficient mice. This may be due to altered Ca 2+ homeostasis in these mice, as compared to wild mouse chromaffin cells.

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“…1996). Ulate et al . (2000) made a study on voltage‐clamped bovine chromaffin cells, measuring I Ca and ΔCm elicited by single 100‐ms depolarizing pulses in 10 m m Ca 2+ .…”

Section: Discussionmentioning

confidence: 99%

“…1991a,b, 1994; Albillos et al . 1993, 1996; Lukyanetz and Neher 1999; Ulate et al . 2000), cat (Albillos et al .…”

Section: Discussionmentioning

confidence: 99%

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice

Aldea

Jun

Shin

et al. 2002

Journal of Neurochemistry

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“…Despite the many reports, convincing proof of a specific co-localization of either one of the expressed Cav channel types with the secretory apparatus is still lacking. Each channel type control catecholamine release with the same Ca 2+ -dependence [6, 40-48]. The question is thus, why chromaffin cells which are spherically shaped cells and do not possess neuron-like morphology and specialized pre-post microdomains need so many different Ca 2+ channel types for their function?…”

Section: Tonic Versus Bursts Firing Mode In Chromaffin Cells: Basic Rmentioning

confidence: 99%

Ca<sub>v</sub>1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells

Vandael¹,

Marcantoni²,

Carbone

2015

CMP

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Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca2+ to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from “tonic” to “burst” firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these “neuron-like” firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress.

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“…Since the discovery that bovine chromaffin cells expressed multiple Ca 2+ channels, efforts have been made to find out a kind of specialization for each channel subtype to drive a specific cell function. For instance, concerning exocytosis, L channels [6,33], PQ channels [36], or all channels [41,69] drive the secretory process. This disparity may be due to different stimuli and experimental conditions used [23].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of N and PQ calcium channels by calcium entry through L channels in chromaffin cells

Rosa

Gandı́a

Garcı́a

2009

Pflugers Arch - Eur J Physiol

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Why adrenal chromaffin cells express various subtypes of voltage-dependent Ca(2+) channels and whether a given channel is specialized to perform a specific function are puzzling and unanswered questions. In this study, we have used the L Ca(2+) channel activator FPL64176 (FPL) to test the hypothesis that enhanced Ca(2+) entry through this channel favors the inhibition of N and PQ channels in voltage-clamped bovine adrenal chromaffin cells. Using 2 mM Ca(2+) as charge carrier and under the perforated-patch configuration (PPC) of the patch-clamp technique, FPL caused a paradoxical inhibition of the whole-cell inward Ca(2+) current (I (Ca)). Such inhibition turned on into an augmentation upon cell loading with EGTA-AM. Also, under the whole-cell configuration (WCC) of the patch-clamp technique, FPL decreased I (Ca) in the absence of EGTA from the pipette solution and increased the current in its presence. Using 2 mM Ba(2+) as charge carrier, FPL augmented the Ba(2+) current under both recording conditions, WCC and PPC. FPL augmented the residual current remaining after blockade of N and PQ channels with omega-conotoxin MVIIC or by holding the membrane potential at -50 mV. The data support the view that Ca(2+) entering the cell through the lesser inactivating L channels serves to modulate the more inactivating N and PQ channels. They also suggest a close colocalization of L and N/PQ Ca(2+) channels. This kind of L channel specialization may be relevant to cell excitability, exocytosis, and cell survival mechanisms.

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Extracellular ATP regulates exocytosis by inhibiting multiple Ca2+ channel types in bovine chromaffin cells

Cited by 20 publications

References 28 publications

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice

Ca<sub>v</sub>1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells

Inhibition of N and PQ calcium channels by calcium entry through L channels in chromaffin cells

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Extracellular ATP regulates exocytosis by inhibiting multiple Ca2+ channel types in bovine chromaffin cells

Cited by 20 publications

References 28 publications

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α1A knockout mice

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α1A knockout mice

Ca<sub>v</sub>1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells

Inhibition of N and PQ calcium channels by calcium entry through L channels in chromaffin cells

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A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice

A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α_1A knockout mice