Ca2+-activated Cl− channel in plasmalemma ofNitellopsis obtusa

Shiina, Takashi; Tazawa, Masashi

doi:10.1007/bf01871233

Cited by 58 publications

(28 citation statements)

References 38 publications

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“…The increased Ca2+ activity might be the trigger that opens ion channels in the plasmalemma to further depolarize the membrane. These could be Caz+-dependent C1-channels, as in characean cells (Lunevsky et al, 1983;Shiina and Tazawa, 1987;Okihara et al, 1991) (see below), or Ca2+-dependent K+ channels, as in Eremosphaeva (Thaler et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

“…C1-seems to play a straightforward part as a depolarizing efflux, the role of Ca2+ is probably more complex (Beilby, 1984). Ca2+ influx across the plasmalemma would depolarize the membrane, yet Ca2+ might also be necessary to open C1-chan els of the plasma membrane, as in characean cells (Lunevsky et al, 1983;Shiina andTazawa, 1987. Okihara et al, 1991).…”

Section: The Lntracellular Ci-and No3-activities and Theirmentioning

confidence: 99%

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Cytoplasmic Ca2+, K+, Cl-, and NO3- Activities in the Liverwort Conocephalum conicum L. at Rest and during Action Potentials

1994

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lntracellular Caz+, K+, CI-, and NOs-activities were measured with ion-selective microeledrodes in the liverwort Conocephalum conicum 1. at rest, during dark/light changes, and in the couese of adion potentials triggered by light or electrical stimuli. l h e average free cytosolic Caz+ concentration was 231 f 65 nM. We did not observe any light-dependent changes of the free cytosolic Caz+ concentration as long as no adion potential was triggered. During adion potentials, on average a 2-fold increase of the free cytoplasmic Caz+ concentration was recorded. lntracellular K+ adivity was 76 f 10 mM. It did not depend on K+ concentration changes in the bath solution between 0.1 and 10 mM. The average equilibrium potential for K+ in the standard medium containing 1 mM K+ was -110 mV, which differed significantly from the resting potentia1 of -151 f 2 mV. During adion potentials, either a slight decrease or no changes in intracellular K+ activity were recorded.The average CI-adivity was 7.4 f 0.2 mM in the cytoplasm and 43.5 f 7 mM in the vacuole. l h e adivities of NO,-were 0.63 I : 0.05 mM in the cytoplasm and 3.0 f 0.3 mM in the vacuole. For both anions the vacuolar activity was 5 to 6 times higher than the cytoplasmic activity. After the light was switched off both the CIand the NOs-adivity showed either no change or a slight increase. lllumination caused a gradual return to previous values or no change. During action potentials a slight decrease of intracellular CI-activity was recorded. It was concluded that in Conocephalum, as in characean cells, chloride channels are involved in the depolarization phase of the action potentials. We discuss a model for the ion fluxes during an action potential in Conocephalum.APs in plants play an important role in intracellular signaling and in the regulation of different physiological processes (Davies, 1987; Dziubifiska et al., 1989;Wildon et al., 1992;Fromm and Spanswick, 1993). To understand the function of APs in plant physiology, their ion mechanism has to be known in detail. Data conceming the sequence of ion fluxes during APs in plants were obtained primarily on the highly specialized giant characean cells (Beilby, 1984).According to the present model, APs in these plants are

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Section: Discussionmentioning

confidence: 99%

Section: The Lntracellular Ci-and No3-activities and Theirmentioning

confidence: 99%

Cytoplasmic Ca2+, K+, Cl-, and NO3- Activities in the Liverwort Conocephalum conicum L. at Rest and during Action Potentials

1994

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“…There is also evidence that Ca 2 + causes the inactivation of a second, nonselective ion channel at the tonoplast (Hedrich & Neher, 1987). The situation at the plasma membrane is equally complex, where high cytoplasmic Ca 2 + inhibits inward-rectifying K + channels in guard cells (Schroeder & Hagiwara, 1989) and also activates a CI conductance in Chara (Shiina & Tazawa, 1987a) and in guard cells (Schroeder & Hagiwara, 1989) in addition to the cation channels described above.…”

Section: Modulation Of the Time-dependent K + Current By Intracellulamentioning

confidence: 97%

Cytosolic calcium regulates a potassium current in corn (Zea mays) protoplasts

Ketchum

Poole

1991

J. Membrain Biol.

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The voltage- and time-dependent K+ current, IK+ out, elicited by depolarization of corn protoplasts, was inhibited by the addition of calcium channel antagonists (nitrendipine, nifedipine, verapamil, methoxyverapamil, bepridil, but not La3+) to the extracellular medium. These results suggested that the influx of external Ca2+ was necessary for K+ current activation. The IC50, concentration of inhibitor that caused 50% reduction of the current, for nitrendipine was 1 microM at a test potential of +60 mV following a 20-min incubation period. In order to test whether intracellular Ca2+ actuated the K+ current, we altered either the Ca2+ buffering capacity or the free Ca2+ concentration of the intracellular medium (pipette filling solution). By these means, IK+out could be varied over a 10-fold range. Increasing the free Ca2+ concentration from 40 to 400 nM also shifted the activation of the K+ current toward more negative potentials. Maintaining cytoplasmic Ca2+ at 500 nM with 40 nM EGTA resulted in a more rapid activation of the K+ current. Thus the normal rate of activation of this current may reflect changes in cytoplasmic Ca2+ on depolarization. Increasing intracellular Ca2+ to 500 nM or 1 microM also led to inactivation of the K+ current within a few minutes. It is concluded that IK+out is regulated by cytosolic Ca2+, which is in turn controlled by Ca2+ influx through dihydropyridine-, and phenylalkylamine-sensitive channels.

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“…CaCCs influence cellular electrical activity from algae to neurons CaCCs have a long evolutionary historyin algae, they are responsible for propagation of the action potential that, following an external stimulus, signals for the cell to terminate its usual protoplasmic streaming (Fromm and Lautner, 2007;Shiina and Tazawa, 1987). In Xenopus oocytes, rapid Cl -efflux through CaCCs that are activated following an encounter with a single sperm depolarizes the membrane, thereby preventing the entry of additional sperm (see poster 'CaCCs regulate membrane potential') (Cross, 1981).…”

Section: CLmentioning

confidence: 99%