Feedback Control of the ATP-Sensitive K+ Current by Cytosolic Ca2+ Contributes to Oscillations of the Membrane Potential in Pancreatic β-Cells

Rolland, Jean-François; Henquin, Jean‐Claude; Gilon, Patrick

doi:10.2337/diabetes.51.2.376

Cited by 47 publications

(56 citation statements)

References 55 publications

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“…This agrees with the recent report that elevated insulin secretion from sur1 −/− islets can be suppressed with NaN 3 [21]. Nenquin et al [21] [23,26]. In addition, it has been shown that increased Ca 2+ influx can induce hyperpolarisation of V m that is not mediated by K ATP channels [39] and that a small Ca 2+ -dependent K + current, referred to as I K,slow , is activated when [Ca 2+ ] i is increased in response to simulated bursts of action potentials [28,30].…”

Section: Discussionsupporting

confidence: 83%

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Crosstalk between membrane potential and cytosolic Ca2+ concentration in beta cells from Sur1−/− mice

et al. 2005

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Section: Discussionsupporting

confidence: 83%

“…During glucose stimulation transient openings of K ATP channels [23,26,27] [8,9]. These oscillations are not driven by glucose metabolism [9].…”

Section: Introductionmentioning

confidence: 99%

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Crosstalk between membrane potential and cytosolic Ca2+ concentration in beta cells from Sur1−/− mice

et al. 2005

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“…Second, K ATP channels have been considered to play a key role in the oscillatory activity of beta cells [24,32,33,34]. For example, it has been reported recently that a rise in [Ca 2+ ] c lowers ATP production evoking an increase in the K ATP currents which act as a negative feedback to reduce Ca 2+ influx by hyperpolarizing the beta cell [35]. In normal beta cells oscillations in [Ca 2+ ] c are thought to be necessary for pulsatile insulin secretion [36].…”

Section: Discussionmentioning

confidence: 99%

Oscillations of membrane potential and cytosolic Ca2+ concentration in SUR1−/− beta cells

et al. 2004

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Aims/hypothesis. SUR1(ABCC8) −/− mice lacking functional K ATP channels are an appropriate model to test the significance of K ATP channels in beta-cell function. We examined how this gene deletion interferes with stimulus-secretion coupling. We tested the influence of metabolic inhibition and galanin, whose mode of action is controversial. Methods. Plasma membrane potential (Vm) and currents were measured with microelectrodes or the patch-clamp technique; cytosolic Ca 2+ concentrations ([Ca 2+ ] c ) and mitochondrial membrane potential (∆Ψ) were measured using fluorescent dyes. Results. In contrast to the controls, SUR1 −/− beta cells showed electrical activity even at a low glucose concentration. Continuous spike activity was measured with the patch-clamp technique, but with microelectrodes slow oscillations in Vm consisting of bursts of Ca 2+ -dependent action potentials were detected.

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“…Two criteria defined previously (17) were used to identify single ␤-cells: a cell capacitance above 5 pF and the presence of a voltage-dependent Na ϩ current that is inactivated at a holding potential of Ϫ70 mV but can be activated after a hyperpolarizing pulse to Ϫ140 mV. Patch-clamp measurements were carried out in both conventional and perforated whole cell modes, using an EPC-9 patch-clamp amplifier (Heka Electronics, Lambrecht/Pfalz, Germany) and the software Pulsefit or an Axopatch 200 B patch-clamp amplifier (Axon Instruments, Foster City, CA) and the software pClamp 8.…”

Section: Methodsmentioning

confidence: 99%

G Protein-independent Activation of an Inward Na+Current by Muscarinic Receptors in Mouse Pancreatic β-Cells

Rolland¹,

Henquin²,

Gilon³

2002

Journal of Biological Chemistry

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Depolarization of pancreatic ␤-cells is critical for stimulation of insulin secretion by acetylcholine but remains unexplained. Using voltage-clamped ␤-cells, we identified a small inward current produced by acetylcholine, which was suppressed by atropine or external Na ؉ omission, but was not mimicked by nicotine, and was insensitive to nicotinic antagonists, tetrodotoxin, 4,4-diisothiocyanostilbene-2,2-disulfonic acid (DiDS), thapsigargin pretreatment, and external Ca 2؉ and K ؉ removal. This suggests that muscarinic receptor stimulation activates voltage-insensitive Na ؉ channels distinct from store-operated channels. No outward Na ؉ current was produced by acetylcholine when the electrochemical Na ؉ gradient was reversed, indicating that the channels are inward rectifiers. No outward K ؉ current occurred either, and the reversal potential of the current activated by acetylcholine in the presence of Na ؉ and K ؉ was close to that expected for a Na ؉ -selective membrane, suggesting that the channels opened by acetylcholine are specific for Na ؉ . Overnight pretreatment with pertussis toxin or the addition of guanosine 5-O-(3-thiotriphosphate) (GTP-␥-S) or guanosine-5-O-(2-thiodiphosphate) (GDP-␤-S) instead of GTP to the pipette solution did not alter this current, excluding involvement of G proteins. Injection of a current of a similar amplitude to that induced by acetylcholine elicited electrical activity in ␤-cells perifused with a subthreshold glucose concentration. These results demonstrate that muscarinic receptor activation in pancreatic ␤-cells triggers, by a G protein-independent mechanism, a selective Na ؉ current that explains the plasma membrane depolarization.

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Feedback Control of the ATP-Sensitive K+ Current by Cytosolic Ca2+ Contributes to Oscillations of the Membrane Potential in Pancreatic β-Cells

Cited by 47 publications

References 55 publications

Crosstalk between membrane potential and cytosolic Ca2+ concentration in beta cells from Sur1−/− mice

Crosstalk between membrane potential and cytosolic Ca2+ concentration in beta cells from Sur1−/− mice

Oscillations of membrane potential and cytosolic Ca2+ concentration in SUR1−/− beta cells

G Protein-independent Activation of an Inward Na+Current by Muscarinic Receptors in Mouse Pancreatic β-Cells

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