Interactions of membrane potential and cations in regulation of ciliary activity in Paramecium

1976 ◽  
Vol 65 (2) ◽  
pp. 427-448
Author(s):  
H. Machemer
Keyword(s):  
Membrane Potential ◽  
High Frequency ◽  
Resting Potential ◽  
Ciliary Activity ◽  
Frequency Increase ◽  
External Concentration ◽  
Membrane Hyperpolarization ◽  
Ciliary Beating ◽  
Fixed Membrane ◽  
K Concentration

Ciliary activity in Paramecium was investigated in different external solutions using techniques of voltage clamp and high frequency cinematography. An increase in the external concentration of K, Ca or Mg ions decreased the resting potential. It had no effect on ciliary activity. When the membrane potential was fixed, an increase in external Ca or Mg and, to a lesser extent, an increase in K concentration, raised the frequency of normal beating or decreased the frequency of reversed beating of the cilia. Similar effects resulted from membrane hyperpolarization with constant ionic conditions. Increase in concentration of Ca, but not of Mg or K, enhanced hyperpolarization-induced augmentation of ciliary frequency. Increase in Ca concentration also specifically augmented the delayed increase in inward current during rapid hyperpolarizing clamp. The results support the view that [Ca]i regulates the frequency and direction of ciliary beating. It is suggested that the insensitivity of the ciliary motor system to elevations of the external concentrations of ions results from compensation of their effects on [Ca]i. Depolarization itself appears to increase [Ca]i while elevation of the external ion concentrations at a fixed membrane potential appears to decrease [Ca]i.

Voltage-dependence of ciliary activity in the ciliate Didinium nasutum

1995 ◽  
Vol 198 (12) ◽  
pp. 2537-2545 ◽  
Author(s):  
J Pernberg ◽  
H Machemer
Keyword(s):  
Membrane Potential ◽  
Voltage Dependence ◽  
Longitudinal Axis ◽  
Threshold Level ◽  
Swimming Behaviour ◽  
Ciliary Activity ◽  
Frequency Increase ◽  
Cyclic Activity ◽  
Beating Frequency ◽  
Ca2 Channels

In the gymnostome ciliate Didinium nasutum, swimming behaviour depends upon the cyclic activity of about 3000 cilia. The normal beating mode, resulting in forward swimming of the cell, is characterized by a posteriad effective beat (18 left of the longitudinal axis) at a frequency of approximately 15 Hz. Activation of depolarization-sensitive ciliary Ca2+ channels leads to an increase in intracellular Ca2+ concentration and a change in the beating mode. Following rapid reorientation, the effective stroke is anteriad (24 ° right of the longitudinal axis) and the beating frequency is about 26 Hz, resulting in fast backward swimming of the cell. In response to minor depolarizations, and hence small increases in cytoplasmic Ca2+ concentration, the cilia inactivate. Frequency increase and reversal in beat orientation share a single threshold level of membrane potential, since both changes of the beating mode occur simultaneously.

Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells

1989 ◽  
Vol 257 (3) ◽  
pp. H778-H784 ◽  
Author(s):  
W. P. Schilling
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Cytosolic Calcium ◽  
Membrane Depolarization ◽  
K Channel ◽  
Membrane Hyperpolarization ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
K Concentration ◽  
Aortic Endothelial

The effect of bradykinin on membrane potential of cultured bovine aortic endothelial cells (BAECs) was estimated by measuring the uptake of the lipophilic cation, tetra[3H]phenylphosphonium ([3H]TPP+). Uptake of [3H]TPP+ was found to be 1) a function of extracellular K+ concentration, 2) sensitive to valinomycin, and 3) decreased by the K+ channel inhibitor, Ba2+, suggesting that the uptake of [3H]TPP+ responds to changes in membrane potential of the BAEC. Bradykinin (50 nM) produced an increase in [3H]TPP+ uptake in low K+ buffer consistent with a bradykinin-induced membrane hyperpolarization. The effect of membrane depolarization with high K+ buffer on the bradykinin-stimulated changes in cytosolic Ca2+ was determined using the fluorescent Ca2+ indicator, fura-2. The results of these experiments demonstrated that both basal cytosolic Ca2+ and bradykinin-stimulated release of Ca2+ from internal stores were not affected by membrane depolarization. However, bradykinin-stimulated influx of Ca2+ from the extracellular space decreased with membrane depolarization in a manner consistent with the movement of Ca2+ through a channel.

Potassium distribution and membrane potential of sensory neurons in the leech nervous system

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

The diffusion and electrogenic components of the membrane potential of hypoxic myocardium

1987 ◽  
Vol 65 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Resting Potential ◽  
Krebs Solution ◽  
Ventricular Muscle ◽  
Diffusion Component ◽  
K Concentration ◽  
Zero Potential ◽  
K Permeability ◽  
External K

The diffusion and electrogenic components of the resting potential of hypoxic ventricular muscle were separated by inhibition of the sodium pump with 10−4 M ouabain. The response to varying external K concentrations (Ko) was studied. Arteriaily perfused rabbit hearts were submitted to 60 min hypoxia in Krebs solution containing 5 mM K throughout or to different external K concentrations during the last 20 min of hypoxia. For K concentrations between 1.5 and 10 mM, hypoxia did not change the resting potential except for a slight hyperpolarization in 7.5 mM K. The diffusion component of the resting potential did not differ from the resting potential at Ko < 5 mM. An electrogenic potential of −3 to −6 mV was detectable at Ko values between 5 and 10 mM. The internal K concentration, Ki, was estimated from extrapolations to zero potential of the relation resting potential vs. Ko in normoxic and hypoxic hearts. These experiments revealed a decline of Ki of 16 mM with hypoxia. The variation of the diffusion potential with external K was fitted by a PNa:PK ratio five times lower than in normoxia. It has been concluded that an increase in K permeability and the persistence of electrogenic Na extrusion during hypoxia of rather short duration prevent membrane depolarization despite the myocardial K loss.

Membrane Control of Ciliary Activity in the Protozoan Euplotes

1973 ◽  
Vol 58 (2) ◽  
pp. 437-462
Author(s):  
MILES EPSTEIN ◽  
ROGER ECKERT
Keyword(s):  
Membrane Potential ◽  
Normal Direction ◽  
Direct Access ◽  
Ciliary Activity ◽  
Cell Interior ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Intracellular Ca ◽  
Triton X ◽  
External Calcium

1. Membrane control of ciliary activity in the protozoan Euplotes was investigated by a combination of electrophysiological and cinematographic techniques. 2. The anal cirri, which are quiescent in the absence of stimulation, were selected for this study. 3. Membrane depolarization by means of injected current produced a reversal of the direction of beating (i.e. towards the cell anterior so as to make the ciliate swim backwards). Depolarization also increased the frequency of beating. Increasing depolarizations resulted in an increased number of reversed beats and increased frequency. 4. When the membrane potential was shifted beyond +70 mV, reversed beating did not occur until after the current pulse ended. 5. Depolarization did not evoke reversed beating when the external calcium (Ca) concentration was reduced to 10-6 M with EGTA. 6. Hyperpolarization caused the cirri to beat in a normal direction (i.e. towards the rear of the ciliate so as to cause the animal to swim forward). Increasing hyperpolarizations resulted in an increased number of forward beats and an increased frequency. 7. The cell was treated with the detergent Triton X-100 to permit Ca, Mg and ATP direct access through the extracted membrane to the cell interior. At Ca concentrations below 10-7 M, Mg-ATP-reactivated cilia of Triton-extracted cells beat normally. At Ca concentrations above approximately 10-7 M the reactivated beat resembled the reversed beat in the living cell. 8. The evidence suggests that membrane-regulated concentrations of intracellular Ca control the direction of ciliary beating. Thus, stimuli which produce an adequate Ca influx lead to ciliary reversal.

scholarly journals Suppression of spikes during posttetanic hyperpolarization in auditory neurons: the role of temperature, Ih currents, and the Na+-K+-ATPase pump

2012 ◽  
Vol 108 (7) ◽  
pp. 1924-1932 ◽  
Author(s):  
Jun Hee Kim ◽  
Henrique von Gersdorff
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Atpase Activity ◽  
Brain Stem ◽  
High Frequency ◽  
Afferent Fiber ◽  
Resting Potential ◽  
Effect Of Temperature ◽  
Resting Membrane Potential ◽  
Temperature Sensitive

In vivo recordings from postsynaptic neurons in the medial nucleus of the trapezoid body (MNTB), an auditory brain stem nucleus, show that acoustic stimulation produces a burst of spikes followed by a period of hyperpolarization and suppressed spiking activity. The underlying mechanism for this hyperpolarization and reduced spiking is unknown. Furthermore, the mechanisms that control excitability and resting membrane potential are not fully determined for these MNTB neurons. In this study we investigated the excitability of principal neurons from the MNTB after high-frequency afferent fiber stimulation, using whole cell recordings from postnatal day 15–17 rat brain stem slices. We found that Na+-K+-ATPase activity mediates a progressive hyperpolarization during a prolonged tetanic train and a posttetanic hyperpolarization (PTH) at the end of the train, when postsynaptic action potentials failed to fire. Raising the temperature to more physiological levels (from 22 to 35°C) depolarized the resting membrane potential of both presynaptic and postsynaptic cells and decreased the latency of action potential firing during PTH. Higher temperatures also reduced the presynaptic calyx action potential failure rates by 50% during presynaptic PTH, thus increasing the safety-factor for presynaptic spiking. The effect of temperature on hyperpolarization-activated cation current ( Ih) is reflected in the resting potential at both pre- and postsynaptic neurons. We thus propose that temperature-sensitive Na+-K+-ATPase activity and Ih contribute to set the resting membrane potential and produce a brief period of suppressed spiking (or action potential failures) after a prolonged high-frequency afferent tetanus.

scholarly journals Pharmacological Study of the Reciprocal Dual Innervation of the Lateral Ciliated Gill Epithelium by the CNS of Mytilus Edulis (Bivalvia)

1978 ◽  
Vol 74 (1) ◽  
pp. 101-113 ◽  
Author(s):  
EDWARD J. CATAPANE ◽  
GEORGE B. STEFANO ◽  
EDWARD AIELLO
Keyword(s):  
Mytilus Edulis ◽  
High Frequency ◽  
Pharmacological Study ◽  
Low Frequency ◽  
High Frequency Stimulation ◽  
Ciliary Activity ◽  
Visceral Ganglion ◽  
Ciliary Beating ◽  
Frequency Stimulation ◽  
Stimulation Of

The function of the CNS of Mytilus edulis was investigated for its role in the control of lateral ciliary activity. Ciliary beating rates were directly measured by stroboscopic microscopy of gill preparations which had the ipsilateral visceral ganglion (VG) attached. Low frequency electrical stimulation of the cerebrovisceral connective (CVC) or superfusion of the VG with serotonin increased lateral ciliary activity. This response could be antagonized by pretreating the gill with BOL or methysergide (MS), or by pretreating the VG with BOL, MS or ergonovine (ERG). High frequency stimulation of the CVC or superfusion of the VG with dopamine or epinephrine decreased lateral ciliary activity. This response could be antagonized by pretreating the gill with ERG or by pretreating the VG with ERG or MS. Acetylcholine and its mimetic acetylmethylcholine were found to be non-effective in altering ciliary activity in this study. The study demonstrates a reciprocal serotonergic-dopaminergic innervation of lateral gill ciliated cells originating in the CNS.

scholarly journals Glucose stimulates voltage- and calcium-dependent inositol trisphosphate production and intracellular calcium mobilization in insulin-secreting β TC3 cells

1996 ◽  
Vol 314 (1) ◽  
pp. 339-345 ◽  
Author(s):  
Jesper GROMADA ◽  
Jørgen FRØKJÆR-JENSEN ◽  
Steen DISSING
Keyword(s):  
Membrane Potential ◽  
Resting Potential ◽  
Glucose Stimulation ◽  
Calcium Dependent ◽  
Cellular Processes ◽  
Intracellular Calcium Mobilization ◽  
Inositol 1,4,5 Trisphosphate ◽  
Voltage Dependent ◽  
K Concentration ◽  
Induced Changes

The cellular processes leading to a rise in the intracellular free Ca2+ concentration ([Ca2+]i) after glucose stimulation and K+ depolarization were investigated in insulin-secreting βTC3 cells. Stimulation with 11.2 mM glucose causes inositol 1,4,5-trisphosphate production and release of Ca2+ from intracellular stores. A strong correlation was observed between the changes in Ins(1,4,5)P3 concentration and the rise in [Ca2+]i, consistent with the former compound being responsible for release of Ca2+ from intracellular stores. The increase in Ins(1,4,5)P3 production was reduced by 68±4% when [Ca2+]i was kept low on glucose stimulation by loading cells with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-NNN´N´-tetra-acetic acid (BAPTA). The Ins(1,4,5)P3 production was prevented in cells hyperpolarized with diazoxide, an opener of ATP-sensitive K+-channels, consistent with the membrane potential controlling the rate of Ins(1,4,5)P3 synthesis. Depolarizing K+ concentrations evoked changes in [Ca2+]i and Ins(1,4,5)P3 production in both the presence and the absence of extracellular Ca2+, and from the relation between the extracellular K+ concentration and membrane potential we found a half-maximal Ins(1,4,5)P3 production by a 28 mV depolarization from a resting potential of -56 mV and by a rise in [Ca2+]i of 390 nM. We conclude that stimulation-induced changes in membrane potential and [Ca2+]i are important in controlling Ins(1,4,5)P3 production in βTC-3 cells and that glucose-stimulated Ca2+ mobilization from intracellular stores is due to voltage-dependent Ins(1,4,5)P3 production and depends on the concurrent increase in [Ca2+]i.

Unidirectional flux ratio for potassium ions in depolarized frog skeletal muscle

1981 ◽  
Vol 241 (1) ◽  
pp. C68-C75 ◽  
Author(s):  
B. C. Spalding ◽  
O. Senyk ◽  
J. G. Swift ◽  
P. Horowicz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Flux Ratio ◽  
External Solution ◽  
Resting Potential ◽  
Frog Skeletal Muscle ◽  
High K ◽  
Sigmoidal Curve ◽  
K Concentration ◽  
Low K

Small bundles of frog skeletal muscle fibers were loaded with 305 mM K+ and 120 mM Cl-, and 42K+ tracer efflux and influx were measured as a function of external K+ concentration ([K+]o) at a resting potential of -2 mV. As [K+]o was lowered from 305 mM, efflux decreased along a markedly sigmoidal curve, reaching a constant nonzero value at low [K+]o. Influx varied linearly with [K+]o at low [K+]o and more steeply at higher [K+]o. The ratio of influx to efflux was described by the equation: influx/efflux = exp[-n(V - VK)F/RT] with n = 2 at high [K+]o, but the ratio approached this equation with n = 1 at low [K+]o. Efflux did not depend on [K+]o when the membrane potential was raised to +36 mV, whereas at low [K+]o decreasing the membrane potential to -19 mV further activated the efflux. The results are discussed in terms of an inwardly rectifying potassium channel with two or more activating sites within the membrane that bind K+ and are accessible from the external solution.

scholarly journals Electrophysiological engineering of heart-derived cells with calcium-dependent potassium channels improves cell therapy efficacy for cardioprotection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Patrick Vigneault ◽  
Sandrine Parent ◽  
Pushpinder Kanda ◽  
Connor Michie ◽  
Darryl R. Davis ◽  
...  
Keyword(s):  
Cell Therapy ◽  
Therapeutic Potential ◽  
Resting Potential ◽  
Intramyocardial Injection ◽  
Membrane Hyperpolarization ◽  
Calcium Dependent ◽  
Cell Functions ◽  
Kca Channels ◽  
Therapy Effectiveness ◽  
Intracellular Ca

AbstractWe have shown that calcium-activated potassium (KCa)-channels regulate fundamental progenitor-cell functions, including proliferation, but their contribution to cell-therapy effectiveness is unknown. Here, we test the participation of KCa-channels in human heart explant-derived cell (EDC) physiology and therapeutic potential. TRAM34-sensitive KCa3.1-channels, encoded by the KCNN4 gene, are exclusively expressed in therapeutically bioactive EDC subfractions and maintain a strongly polarized resting potential; whereas therapeutically inert EDCs lack KCa3.1 channels and exhibit depolarized resting potentials. Somatic gene transfer of KCNN4 results in membrane hyperpolarization and increases intracellular [Ca2+], which boosts cell-proliferation and the production of pro-healing cytokines/nanoparticles. Intramyocardial injection of EDCs after KCNN4-gene overexpression markedly increases the salutary effects of EDCs on cardiac function, viable myocardium and peri-infarct neovascularization in a well-established murine model of ischemic cardiomyopathy. Thus, electrophysiological engineering provides a potentially valuable strategy to improve the therapeutic value of progenitor cells for cardioprotection and possibly other indications.

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