P-type calcium channels blocked by the spider toxin ω-Aga-IVA

Mintz, Isabelle M.; Venema, Virginia J.; Swiderek, Kristine M.; Lee, Terry D.; Bean, Bruce P.; Adams, Michael E.

doi:10.1038/355827a0

Cited by 837 publications

(469 citation statements)

References 46 publications

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“…dependent calcium channels, activated calcium channels are blocked specifiand inactivated at a high membrane cally by o-conotoxin GVIA and the funpotential, are the best-characterized plasnel web spider toxin o-Aga-IVA, malemmal calcium entry pathway, prirespectively (Mintz et al 1992). Both marily because of the existence of channels have been identified only in powerful and specific channel-blocking neurons and neuroendocrine cells.…”

mentioning

confidence: 99%

Tissue-specific expression of calcium channels

Hullin¹,

Biel²,

Flockerzi³

et al. 1993

Trends in Cardiovascular Medicine

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mentioning

confidence: 99%

Tissue-specific expression of calcium channels

Hullin¹,

Biel²,

Flockerzi³

et al. 1993

Trends in Cardiovascular Medicine

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“…Using electrophysiological techniques, the presence of L- [9,10], N- [11] and P- [12] type voltage-dependent Ca 2+ channels located on the plasma membrane of chromaffin cells has been demonstrated. P-Type voltage-dependent Ca 2+ channels have been described to carry a significant amount of voltage-activated Ca 2+ current in different neural cells [13][14][15], and have also been implicated in neurotransmitter secretion in different systems [16,17]. In adrenergic tissues, P-type voltage-dependent Ca 2+ channels seem to contribute significantly to Ca 2+ currents in response to depolarization [12].…”

Section: Introductionmentioning

confidence: 99%

ω‐agatoxin IVA blocks nicotinic receptor channels in bovine chromaffin cells

et al. 1995

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We have studied the contribution of P-type voltagedependent Ca 2+ channels to both catacholamine (CA) and ATP secretion from bovine chromaffin cells induced by high K ÷ or nicotine using ¢o-agatoxin IVA, a selective blocker of P-type voltage-dependent Ca 2÷ channels. We found that high K ÷ (75 raM) induced the release of about 13% of norepinephrine, 5% epinephrine and 11% ATP, and that ¢o-agatoxin (100 nM) did not affect this secretion. However, both nicotine-induced CA and ATP secretion were significantly blocked (about 50%) by ¢o-agatoxin IVA (100 nM). In addition, this toxin also reversibly blocked (about 70%) the inward current induced by nicotine in bovine chromaffin cells. The results suggest that, besides its known action of blocking P-type voltage-dependent channels, ¢o-agatoxin is a potent and reversible blocker of the nicotinic receptor channel in chromaffin cells, and that this action would explain the blockade of nicotine-induced secretion.

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“…The single non-L-, non-N-type channel: Q-like versus P-type Of the three non-L-, non-N-type channels described in central neurons (Q, P and R; [12,21,26]) the one observed in RINm5F cells seems more closely related to the Q-type. The R-type channel described in rat cerebellar granules has kinetic properties sharply different from those illustrated here.…”

Section: Discussionmentioning

confidence: 98%

“…Also the Ptype channel is unlikely to correspond to the non-L-, non-N-type observed in RINm5F cells. P-Type channels in cerebellar Purkinje neurons are reported to activate at relatively low membrane potentials (930 to 920 mV in 10 mM Ba 2+ ; [21]) and to exhibit negligible steady-state inactivation at holding potentials of 940 to 960 mV [34], whereas the non-L-, non-N-type channel in RINm5F cells activates positive to 0 mV and is significantly inactivated at a holding potential of 950 mV [18]. Single P-type channels are also reported to be inhibited by Ca 2+ channel agonists [34].…”

Section: Discussionmentioning

confidence: 99%

A single non-L-, non-N-type Ca2+ channel in rat insulin-secreting RINm5F cells

Magnelli¹,

Avaltroni²,

Carbone³

1996

Pflugers Arch.

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Single high-voltage-activated (HVA) Ca 2+ channel activity was recorded in rat insulinoma RINm5F cells using cell-attached and outside-out configurations. Single-channel recordings revealed three distinct Ca 2+ channel subtypes : one sensitive to dihydropyridines (DHPs)-(L-type), another sensitive to -conotoxin (CTx)-GVIA (N-type) and a third type insensitive to DHPs and -CTx-GVIA (non-L-, non-N-type). The L-type channel was recorded in most patches between 930 and +30 mV. The channel had pharmacological and biophysical features similar to the L-type channels described in other insulin-secreting cells (mean conductance 21 pS in control conditions and 24 pS in the presence of 5 µM Bay K 8644). The non-L-, non-N-type channel was recorded in cells chronically treated with -CTx-GVIA in the presence of nifedipine to avoid the contribution of N-and L-type channels. Channel activity was hardly detectable below 910 mV and was recruited by negative holding potentials (< 990 mV). The channel open probability increased steeply from 910 to + 40 mV. Different unitary current sublevels could be detected and the current voltage relationship was calculated from the higher amplitude level with a slope conductance of 21 pS. Channel activity lasted throughout depolarizations of 300-800 ms with little sign of inactivation. Above 0 mV the channel showed a persistent flickering kinetics with brief openings ( o 0.6 ms) and long bursts ( burst 60 ms) interrupted by short interburst intervals. The third HVA Ca 2+ channel subtype, the N-type, had biophysical properties similar to the non-L-, non-N-type and was best identified in outside-out patches by its sensitivity to -CTx-GVIA. The channel was detectable only above 910 mV from a 990 mV holding potential, exhibited a fast flickering behaviour, persisted during prolonged depolarizations and had a slope conductance of about 19 pS. The present data provide direct evidence for a slowly inactivating non-L-, non-N-type channel in insulin-secreting RINm5F cells that activates at more positive voltages than the L-type channel and indicate the possibility of identifying unequivocally single HVA Ca 2+ channels in cellattached and excised membrane patches under controlled pharmacological conditions.

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P-type calcium channels blocked by the spider toxin ω-Aga-IVA

Cited by 837 publications

References 46 publications

Tissue-specific expression of calcium channels

Tissue-specific expression of calcium channels

ω‐agatoxin IVA blocks nicotinic receptor channels in bovine chromaffin cells

A single non-L-, non-N-type Ca2+ channel in rat insulin-secreting RINm5F cells

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