Pertussis toxin stimulation of catecholamine release from adrenal medullary chromaffin cells: Mechanism may be by direct activation of L-type and G-type calcium channels

Ceña, Valentı́n; Brocklehurst, Keith; Pollard, Harvey B.; Rojas, Eduardo

doi:10.1007/bf01872736

Cited by 20 publications

(3 citation statements)

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“…A regulatory role for G proteins in secretory activity of chromaffin cells has already been postulated by Ceina, Brocklehurst, Pollard & Rojas (1991) who have reported increased catecholamine secretion in PTX-treated cells resulting from the removal of the tonic inhibition of Gi/G0 subset of regulatory proteins on the Caa2+ channels.…”

Section: G Protein Regulation Of Atp Effectmentioning

confidence: 72%

ATP modulation of calcium channels in chromaffin cells.

Gandı́a

Garcı́a

Morad

1993

The Journal of Physiology

105

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SUMMARY1. The effects of externally applied micromolar concentrations of adenosine 5'-triphosphate (ATP) on Ca2+ currents (ICa) were studied in whole-cell clamped adrenaline-secreting chromaffin cells.2. Ca2+ currents in chromaffin cells activated at about -40 mV, reached a maximum at 0 mV and had an apparent reversal potential at + 50 to + 60 mV, indicating the existence of only high voltage-activated Ca2+ channels.3. ATP blocked Ca2+ current rapidly, reversibly and in a concentration-dependent manner (10-9-l0-4 M).4. ATP did not completely block Ca2+ current even at the highest concentrations used (100 /LM). The remaining component of Ca2+ current was characterized by slower activation and inactivation kinetics.5. ATP blocked ICa even in the presence of nisoldipine and/or o-conotoxin GVIA, suggesting that its modulatory role is not specific for L-and/or N-type Caa2+ channels.6. Other adenine nucleotides also blocked the Ca2+ current partially. The order of potencies was ATP > ADP > AMP > adenosine, indicating that the ATP effects are most probably mediated by a P2-type purinergic receptor.7. Dialysis of the cells with an intracellular solution containing 1 mm guanosine 5'-O-thiodiphosphate (GDP-,-S) or pre-incubation of the cells with pertussis toxin (PTX) blocked the inhibitory effects of ATP.8. Intracellular application of the non-hydrolysable GTP analogue guanosine 5'-0-(3'-thiotriphosphate) (GTP-y-S; 50 ftM) also decreased ICa in a manner similar to that seen for ATP and significantly reduced the ATP inhibitory effect.

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Section: G Protein Regulation Of Atp Effectmentioning

confidence: 72%

ATP modulation of calcium channels in chromaffin cells.

Gandı́a

Garcı́a

Morad

1993

The Journal of Physiology

105

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“…A metabolically regulated Ca 2+ channel with low voltage dependence was recently described in human β-cells (21). These G-type VICCs have also been described in bovine chromaffin cells, where they were shown to be activated by pertussis toxin (33). Although G-type Ca 2+ channels have not been directly recorded in rat β-cells, the dependence of slow [Ca 2+ ] i oscillations on glucose metabolism and extracellular Ca 2+ may be explained by the influx of Ca 2+ through such a channel.…”

Section: Discussionmentioning

confidence: 85%

Voltage-independent calcium channels mediate slow oscillations of cytosolic calcium that are glucose dependent in pancreatic beta-cells.

1994

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Pancreatic beta-cells and HIT-T15 cells exhibit oscillations of cytosolic calcium ([Ca2+]i) that are dependent on glucose metabolism and appear to trigger pulsatile insulin secretion. Significantly, differences in the pattern of this [Ca2+]i oscillatory activity may have important implications for our understanding of how glucose homeostasis is achieved during the feeding and fasting states. When single beta-cells are exposed to a stepwise increase in glucose concentration that mimics the transition from fasting to feeding states, fast irregular oscillations of [Ca2+]i are observed. Alternatively, when single beta-cells are equilibrated in a steady state concentration of glucose that mimics the fasting state, slow periodic oscillations of [Ca2+]i are noted. Here we report a fundamental difference in the mechanism by which glucose induces these two types of [Ca2+]i oscillatory activity. In agreement with previous studies, we substantiate a role for L-type voltage-dependent Ca2+ channels as mediators of the fast oscillations of [Ca2+]i observed after a stepwise increase in glucose concentration. In marked contrast, we report that voltage-independent calcium channels (VICCs) mediate slow oscillations of [Ca2+]i that occur when beta-cells are equilibrated in steady state concentrations of glucose. Slow [Ca2+]i oscillations are mediated by VICCs which are pharmacologically and biophysically distinguishable from voltage-dependent Ca2+ channels that mediate fast oscillations. Specifically, slow [Ca2+]i oscillations are blocked by extracellular La3+, but not by nifedipine, and are independent of changes in membrane potential. Measurement of membrane conductance also indicate an important role for VICCs, as demonstrated by a steady state inward Ca2+ current that is blocked by La3+. The steady state Ca2+ current appears to generate slow [Ca2+]i oscillations by triggering Ca(2+)-induced Ca2+ release from intracellular Ca2+ stores, a process that is mimicked by extracellular application of caffeine, a sensitizer of the ryanodine receptor/Ca2+ release channel. Depletion of intracellular Ca2+ stores with thapsigargin stimulated Mn2+ influx, suggesting the presence of Ca(2+)-release-activated Ca2+ channels. Taken together, these observations are consistent with a role for VICCs (possibly G-type channels) and/or Ca(2+)-release-activated Ca2+ channels as mediators of slow [Ca2+]i oscillations in beta-cells. We propose that slow oscillations of [Ca2+]i probably serve as important initiators of insulin secretion under conditions in which tight control of glucose homeostasis is necessary, as is the case during the fasting normoglycemic state.

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“…1B). The magnitude of the prepulse facilitation was unaffected by prior addition of naloxone and suramin ( Voltage-dependent (prepulse) facilitation in chromaffin cells is pertussis toxin (PTX)-sensitive (26,29,30). We examined whether the voltage-independent inhibition mediated by purinergic and opioid receptors was PTX-sensitive by comparison with effects of PTX treatment on prepulse facilitation.…”

Section: Voltage-dependent Inhibition Of Camentioning

confidence: 99%

Voltage-independent Inhibition of P/Q-type Ca2+Channels in Adrenal Chromaffin Cells via a Neuronal Ca2+Sensor-1-dependent Pathway Involves Src Family Tyrosine Kinase

Weiss

Burgoyne

2001

Journal of Biological Chemistry

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In common with many neurons, adrenal chromaffin cells possess distinct voltage-dependent and voltage-independent pathways for Ca 2؉ channel regulation. In this study, the voltage-independent pathway was revealed by addition of naloxone and suramin to remove tonic blockade of Ca 2؉ currents via opioid and purinergic receptors due to autocrine feedback inhibition. This pathway requires the Ca 2؉ -binding protein neuronal calcium sensor-1 (NCS-1). The voltage-dependent pathway was pertussis toxin-sensitive, whereas the voltageindependent pathway was largely pertussis toxin-insensitive. Characterization of the voltage-independent inhibition of Ca 2؉ currents revealed that it did not involve protein kinase C-dependent signaling pathways but did require the activity of a Src family tyrosine kinase. Two structurally distinct Src kinase inhibitors, 4-amino-5-(4-methylphenyl)7-(t-butyl)pyrazolo[3,4-d] pyrimidine (PP1) and a Src inhibitory peptide, increased the Ca 2؉ currents, and no further increase in Ca 2؉ currents was elicited by addition of naloxone and suramin. In addition, the Src-like kinase appeared to act in the same pathway as NCS-1. In contrast, addition of PP1 did not prevent a voltage-dependent facilitation elicited by a strong pre-pulse depolarization indicating that this pathway was independent of Src kinase activity. PPI no longer increased Ca 2؉ currents after addition of the P/Q-type channel blocker -agatoxin TK. The ␣ 1A subunit of P/Q-type Ca 2؉ channels was immunoprecipitated from chromaffin cell extracts and found to be phosphorylated in a PP1-sensitive manner by endogenous kinases in the immunoprecipitate. A high molecular mass (around 220 kDa) form of the ␣ 1A subunit was detected by anti-phosphotyrosine, suggesting a possible target for Src family kinase action. These data demonstrate a voltage-independent mechanism for autocrine inhibition of P/Q-type Ca 2؉ channel currents in chromaffin cells that requires Src family kinase activity and suggests that this may be a widely distributed pathway for Ca 2؉ channel regulation.

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Pertussis toxin stimulation of catecholamine release from adrenal medullary chromaffin cells: Mechanism may be by direct activation of L-type and G-type calcium channels

Cited by 20 publications

References 20 publications

ATP modulation of calcium channels in chromaffin cells.

ATP modulation of calcium channels in chromaffin cells.

Voltage-independent calcium channels mediate slow oscillations of cytosolic calcium that are glucose dependent in pancreatic beta-cells.

Voltage-independent Inhibition of P/Q-type Ca2+Channels in Adrenal Chromaffin Cells via a Neuronal Ca2+Sensor-1-dependent Pathway Involves Src Family Tyrosine Kinase

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