Ca-dependent K channels with large unitary conductance in chromaffin cell membranes

Marty, Alain

doi:10.1038/291497a0

Cited by 631 publications

(440 citation statements)

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“…Ca 2+ -activated K + currents: The model includes two Ca 2+ -activated K + currents mediated by SK and BK channels (Marty 1981;Marty and Neher 1985;Vergara et al 1998). Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999).…”

Section: (A)mentioning

confidence: 99%

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

2007

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Magnocellular neuroendocrine cells (MNCs) of the hypothalamus synthesize the neurohormones vasopressin and oxytocin, which are released into the blood and exert a wide spectrum of actions, including the regulation of cardiovascular and reproductive functions. Vasopressin-and oxytocinsecreting neurons have similar morphological structure and electrophysiological characteristics. A realistic multicompartmental model of a MNC with a bipolar branching structure was developed and calibrated based on morphological and in vitro electrophysiological data in order to explore the roles of ion currents and intracellular calcium dynamics in the intrinsic electrical MNC properties. The model was used to determine the likely distributions of ion conductances in morphologically distinct parts of the MNCs: soma, primary dendrites and secondary dendrites. While reproducing the general electrophysiological features of MNCs, the model demonstrates that the differential spatial distributions of ion channels influence the functional expression of MNC properties, and reveals the potential importance of dendritic conductances in these properties.

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Section: (A)mentioning

confidence: 99%

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

2007

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“…MEECH (1972) first observed the Ca-activated increase of K permeability in Aplysia nerve cells. Studies on Ca-activated K currents have been performed at the single channel level in neurons, smooth muscle, chromaffin cells, and skeletal muscle (MEECH, 1974(MEECH, , 1978THOMPSON, 1977;MIRONNEAU and SAVINEAU, 1980;MARTY, 1981;BARRETT et al, 1982). In cardiac tissues also, ISENBERG (1977a, b) showed the evidence of the Ca-activated K conductance in sheep Purkinje fibers.…”

Section: Js-actions On Cardiac Membrane Currents 525mentioning

confidence: 99%

.BETA.-Actions of catecholamines on the K-related currents of the bullfrog atrial muscle.

Umeno

1984

Jpn.J.Physiol

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Effects of catecholamines on K-related membrane currents in the bullfrog atrial muscle were studied under voltage clamp using the double sucrose-gap technique. Isoproterenol (10-8l0_6 M) and norepinephrine (5 x 10-6-10-5 M) induced an outward shift of the basal current level and enhanced both the background current (Ib) for hyperpolarization and the instantaneous outward current for depolarization. There was an augmentation of the slow inward current (Isi) and the delayed outward current (Ij.The augmentation of I, was induced with or without an increase in Isi, but different kinetics were involved. In the presence of Isi, j3-agonists produced a more marked augmentation of I, for the intermediate voltages of depolarization where Isi was enhanced, and Co eliminated these effects. In the absence of Isi with Co, j3-agonists elicited an enhancement of Ig; however, the enhancement was greater for larger and longer depolarizations. All these effects were absent in the presence of propranolol (5 x 10-7 M). These observations indicate that j3-agonists directly increase the background K current, and enhance the delayed outward current (Is) via two different mechanisms; one is related to the augmentation of Isi and the other is not.

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“…From the moment we discovered its existence in a membrane preparation from muscle T-tubule (Latorre et al, 1982), we were confronted with a molecular Pandora's box: once opened, its electrical language left all of us bewitched. Others (e.g., Marty, 1981;Pallota et al, 1981) were as fascinated as we were with this "monster" of a single-channel conductance closed to the ceiling imposed by simple diffusion combined with an exquisite K + selectivity. BK channels essentially are impermeant to Na + and conduct K + 10-and 200-fold more effectively than Rb + and Cs + , respectively (large conductance channels were not supposed to be so selective!)…”

Section: Introductionmentioning

confidence: 99%

“…The increase in internal Ca 2+ , however, also puts into action a negative feedback that will serve to stop or to dampen excitatory phenomena induced by the opening of VDCCs. This negative feedback appears as a consequence of the activation of BK (about 250 pS in 100 mM symmetrical KCl;Marty, 1981;Pallota et al, 1981;Latorre et al, 1982; for reviews see Latorre et al, 1989;McManus, 1991). Thus, BK channels have the largest single-channel conductance of all K + selective channels.…”

Section: Introductionmentioning

confidence: 99%

Large conductance Ca2+-activated K+ (BK) channel: Activation by Ca2+ and voltage

2006

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Large conductance Ca 2+ -activated K + (BK) channels belong to the S4 superfamily of K + channels that include voltage-dependent K + (Kv) channels characterized by having six (S1-S6) transmembrane domains and a positively charged S4 domain. As Kv channels, BK channels contain a S4 domain, but they have an extra (S0) transmembrane domain that leads to an external NH 2 -terminus. The BK channel is activated by internal Ca 2+ , and using chimeric channels and mutagenesis, three distinct Ca 2+ -dependent regulatory mechanisms with different divalent cation selectivity have been identified in its large COOH-terminus. Two of these putative Ca 2+ -binding domains activate the BK channel when cytoplasmic Ca 2+ reaches micromolar concentrations, and a low Ca 2+ affinity mechanism may be involved in the physiological regulation by Mg 2+ . The presence in the BK channel of multiple Ca 2+ -binding sites explains the huge Ca 2+ concentration range (0.1 μM-100 μM) in which the divalent cation influences channel gating. BK channels are also voltage-dependent, and all the experimental evidence points toward the S4 domain as the domain in charge of sensing the voltage. Calcium can open BK channels when all the voltage sensors are in their resting configuration, and voltage is able to activate channels in the complete absence of Ca 2+ . Therefore, Ca 2+ and voltage act independently to enhance channel opening, and this behavior can be explained using a two-tiered allosteric gating mechanism.

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Ca-dependent K channels with large unitary conductance in chromaffin cell membranes

Cited by 631 publications

References 11 publications

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

.BETA.-Actions of catecholamines on the K-related currents of the bullfrog atrial muscle.

Large conductance Ca2+-activated K+ (BK) channel: Activation by Ca2+ and voltage

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