Augmentation and suppression of action potentials by estradiol in the myometrium of pregnant rat

1999 ◽  
Vol 77 (6) ◽  
pp. 447-453 ◽  
Author(s):  
Yoshihito Inoue ◽  
Koji Okabe ◽  
Hiroyuki Soeda
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Single Cells ◽  
Muscle Cells ◽  
Enzymatic Digestion ◽  
Resting Membrane Potential ◽  
Spike Generation ◽  
Pregnant Rat ◽  
Outward Currents ◽  
Spontaneous Action

The purpose of this study was to investigate the actions of estradiol on spontaneous and evoked action potentials in the isolated longitudinal smooth muscle cells of the pregnant rat. Single cells were obtained by enzymatic digestion from pregnant rat longitudinal myometrium. Action potentials and currents were recorded by whole-cell current-clamp and voltage-clamp methods, respectively. The acute effects of 17β-estradiol on action potentials and inward and outward currents were investigated. The following results were obtained. The average resting membrane potential of single myometrial cells was -54 mV (n = 40). In many cells, an electrical stimulation evoked a membrane depolarization, and action potentials were superimposed on the depolarization. In some cells, spontaneous action potentials were observed. Estradiol (30 µM) slightly depolarized the membrane (ca. 5 mV) and attenuated the generation of action potentials by reducing the frequency and amplitude of the spikes. Afterhyperpolarization was also attenuated by estradiol (30 µM). On the other hand, in 5 of 35 cells, estradiol increased the first spike amplitude and action potential duration, while frequency of the spike generation and afterhyperpolarization were inhibited. In voltage-clamped muscle cells, estradiol inhibited both inward and outward currents. Acute inhibition or augmentation of spike generation by estradiol is due to the balance of inhibition of inward and outward currents. Inhibition of both currents also prevented afterhyperpolarization, causing potential-dependent block of Ca spikes.Key words: estradiol, progesterone, rat myometrium, action potential, channel current.

Effect of isoprenaline, carbachol, and Cs+ on Na+ activity and pacemaker potential in rabbit SA node cells

1999 ◽  
Vol 276 (1) ◽  
pp. H205-H214 ◽  
Author(s):  
Ho S. Choi ◽  
Dai Y. Wang ◽  
Denis Noble ◽  
Chin O. Lee
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Single Cells ◽  
Sa Node ◽  
Spontaneous Action ◽  
Sodium Binding ◽  
Potential Cycle ◽  
Spontaneous Action Potentials ◽  
Potential Rate ◽  
Zd 7288

Effects of isoprenaline, carbachol, and Cs+on intracellular Na+ activity ([Formula: see text]) and spontaneous action potentials were studied in multicellular and single cell preparations isolated from rabbit sinoatrial (SA) nodes.[Formula: see text] was measured with double-barreled Na+-selective microelectrodes and the fluorescent Na+-indicator sodium-binding benzofuran isophthalate (SBFI). In spontaneously beating cells,[Formula: see text] measured with Na+-selective microelectrodes and SBFI were 4.5 ± 1.2 mM (means ± SD, n = 21) in multicellular preparations and 4.0 ± 1.1 mM ( n = 16) in single cells, respectively. Measurements of[Formula: see text] with microelectrodes showed that isoprenaline increased[Formula: see text] from 4.7 ± 1.2 to 5.5 ± 1.6 mM ( n = 16, P < 0.01) and shortened the action potential cycle length (ACL) from 338 ± 46 to 269 ± 35 ms ( n = 16, P < 0.01). However, increasing the action potential rate by pacing produced a much smaller increase in[Formula: see text]. Changes in[Formula: see text] and ACL produced by isoprenaline were blocked by Cs+. The selective hyperpolarization-activated inward current ( I f) blocker ZD-7288 decreased [Formula: see text] from 5.2 ± 1.0 to 4.6 ± 1.3 mM ( n = 4, P < 0.01) and prolonged ACL from 394 ± 20 to 553 ± 68 ms ( n = 4, P < 0.01). The I f blocker substantially inhibited the increase in[Formula: see text] produced by isoprenaline. Carbachol and Cs+ decreased[Formula: see text] from 4.6 ± 1.4 to 3.9 ± 1.2 mM ( n = 15, P < 0.01) and from 4.9 ± 1.0 to 3.9 ± 1.3 mM ( n = 18, P < 0.01), respectively. In addition, carbachol and Cs+prolonged ACL from 345 ± 44 to 587 ± 100 ms ( n = 15, P < 0.01) and from 353 ± 30 to 464 ± 87 ms ( n = 18, P < 0.01), respectively. However, carbachol and Cs+ almost did not change [Formula: see text] when SA node cells became quiescent in a 25.4 mM extracellular K+ concentration. The results suggest that isoprenaline, ZD-7288, carbachol, or Cs+ might have changed[Formula: see text] and action potential rate by possibly stimulating or inhibiting I f carried by Na+. Measurements of[Formula: see text] with SBFI showed that isoprenaline, carbachol, and Cs+produced [Formula: see text] changes that were similar to those measured with the microelectrodes.

Molecular physiology of cardiac potassium channels

1996 ◽  
Vol 76 (1) ◽  
pp. 49-67 ◽  
Author(s):  
K. K. Deal ◽  
S. K. England ◽  
M. M. Tamkun
Keyword(s):  
Potassium Channels ◽  
Action Potential ◽  
Single Channel ◽  
Resting Membrane Potential ◽  
Molecular Physiology ◽  
K Channels ◽  
Relative Contribution ◽  
Outward Currents ◽  
Important Challenge ◽  
Heterologous Expression Systems

The cardiac action potential results from the complex, but precisely regulated, movement of ions across the sarcolemmal membrane. Potassium channels represent the most diverse class of ion channels in heart and are the targets of several antiarrhythmic drugs. Potassium currents in the myocardium can be classified into one of two general categories: 1) inward rectifying currents such as IK1, IKACh, and IKATP; and 2) primarily voltage-gated currents such as IKs, IKr, IKp, IKur, and Ito. The inward rectifier currents regulate the resting membrane potential, whereas the voltage-activated currents control action potential duration. The presence of these multiple, often overlapping, outward currents in native cardiac myocytes has complicated the study of individual K+ channels; however, the application of molecular cloning technology to these cardiovascular K+ channels has identified the primary structure of these proteins, and heterologous expression systems have allowed a detailed analysis of the function and pharmacology of a single channel type. This review addresses the progress made toward understanding the complex molecular physiology of K+ channels in mammalian myocardium. An important challenge for the future is to determine the relative contribution of each of these cloned channels to cardiac function.

Role of HERG-like K+ currents in opossum esophageal circular smooth muscle

1999 ◽  
Vol 277 (6) ◽  
pp. C1284-C1290 ◽  
Author(s):  
Hamid I. Akbarali ◽  
Hemant Thatte ◽  
Xue Dao He ◽  
Wayne R. Giles ◽  
Raj K. Goyal
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Single Cells ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Circular Smooth Muscle ◽  
Inward Currents

An inwardly rectifying K+ conductance closely resembling the human ether-a-go-go-related gene (HERG) current was identified in single smooth muscle cells of opossum esophageal circular muscle. When cells were voltage clamped at 0 mV, in isotonic K+ solution (140 mM), step hyperpolarizations to −120 mV in 10-mV increments resulted in large inward currents that activated rapidly and then declined slowly (inactivated) during the test pulse in a time- and voltage- dependent fashion. The HERG K+ channel blockers E-4031 (1 μM), cisapride (1 μM), and La3+ (100 μM) strongly inhibited these currents as did millimolar concentrations of Ba2+. Immunoflourescence staining with anti-HERG antibody in single cells resulted in punctate staining at the sarcolemma. At membrane potentials near the resting membrane potential (−50 to −70 mV), this K+ conductance did not inactivate completely. In conventional microelectrode recordings, both E-4031 and cisapride depolarized tissue strips by 10 mV and also induced phasic contractions. In combination, these results provide direct experimental evidence for expression of HERG-like K+ currents in gastrointestinal smooth muscle cells and suggest that HERG plays an important role in modulating the resting membrane potential.

Contribution of Nav1.8 Sodium Channels to Action Potential Electrogenesis in DRG Neurons

2001 ◽  
Vol 86 (2) ◽  
pp. 629-640 ◽  
Author(s):  
Muthukrishnan Renganathan ◽  
Theodore R. Cummins ◽  
Stephen G. Waxman
Keyword(s):  
Action Potential ◽  
Sodium Channels ◽  
Action Potentials ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Drg Neurons ◽  
Significant Difference ◽  
Steady State Inactivation ◽  
Current Threshold

C-type dorsal root ganglion (DRG) neurons can generate tetrodotoxin-resistant (TTX-R) sodium-dependent action potentials. However, multiple sodium channels are expressed in these neurons, and the molecular identity of the TTX-R sodium channels that contribute to action potential production in these neurons has not been established. In this study, we used current-clamp recordings to compare action potential electrogenesis in Nav1.8 (+/+) and (−/−) small DRG neurons maintained for 2–8 h in vitro to examine the role of sodium channel Nav1.8 (α-SNS) in action potential electrogenesis. Although there was no significant difference in resting membrane potential, input resistance, current threshold, or voltage threshold in Nav1.8 (+/+) and (−/−) DRG neurons, there were significant differences in action potential electrogenesis. Most Nav1.8 (+/+) neurons generate all-or-none action potentials, whereas most of Nav1.8 (−/−) neurons produce smaller graded responses. The peak of the response was significantly reduced in Nav1.8 (−/−) neurons [31.5 ± 2.2 (SE) mV] compared with Nav1.8 (+/+) neurons (55.0 ± 4.3 mV). The maximum rise slope was 84.7 ± 11.2 mV/ms in Nav1.8 (+/+) neurons, significantly faster than in Nav1.8 (−/−) neurons where it was 47.2 ± 1.3 mV/ms. Calculations based on the action potential overshoot in Nav1.8 (+/+) and (−/−) neurons, following blockade of Ca2+ currents, indicate that Nav1.8 contributes a substantial fraction (80–90%) of the inward membrane current that flows during the rising phase of the action potential. We found that fast TTX-sensitive Na+ channels can produce all-or-none action potentials in some Nav1.8 (−/−) neurons but, presumably as a result of steady-state inactivation of these channels, electrogenesis in Nav1.8 (−/−) neurons is more sensitive to membrane depolarization than in Nav1.8 (+/+) neurons, and, in the absence of Nav1.8, is attenuated with even modest depolarization. These observations indicate that Nav1.8 contributes substantially to action potential electrogenesis in C-type DRG neurons.

Isolated Giant Smooth Muscle Fibres in Beroe Ovata: Ionic Dependence of Action Potentials Reveals Two Distinct Types of Fibre

1988 ◽  
Vol 135 (1) ◽  
pp. 343-362 ◽  
Author(s):  
ANDRÉ BILBAUT ◽  
ROBERT W. MEECH ◽  
MARI-LUZ HERNANDEZ-NICAISE
Keyword(s):  
Smooth Muscle ◽  
Action Potential ◽  
Action Potentials ◽  
Marine Invertebrate ◽  
The Body ◽  
Fibre Types ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Beroe Ovata ◽  
Radial Muscle

1. The ionic dependence of action potentials evoked in giant smooth muscle fibres isolated by enzymatic digestion from the body wall of the marine invertebrate Beroe ovata (Ctenophora) has been investigated using conventional electrophysiological techniques. 2. Differences were observed in the two fibre types studied. The resting membrane potential was −60 ± 1.35 mV (N = 25) in longitudinal muscle fibres and −66 ±1.37 mV (N=32) in radial fibres. Action potentials had a short plateau in longitudinal fibres but not in radial fibres. 3. The action potential overshoot of both fibre types was decreased in Ca2+-free artificial sea water (ASW). In Na+-deficient ASW, action potentials could not be generated in radial fibres and showed a reduced overshoot in longitudinal fibres. 4. Tetrodotoxin (10−5moll−5) added to ASW or Ca2+-free ASW did not affect the action potentials of either type of fibre. 5. Action potentials of both fibres were partially blocked by Co2+ (20–50 mmoll−1) or Cd2+ (l-2mmoll−1). Action potentials of longitudinal fibres in Na+-deficient ASW were abolished by Co2+ (20mmoll−1). In Ca2+-free ASW, the ction potential overshoots of both sets of fibres were restored following the addition of Sr2+ or Ba2+. In longitudinal fibres, Sr2+ increased the duration of the action potential plateau. In both longitudinal and radial muscle fibres, Ba2+ prolonged the action potential. 6. In longitudinal fibres exposed to tetraethylammonium chloride (TEAC1) or 4-aminopyridine (4AP), the action potential was slightly prolonged. In these fibres, TEA+ or 4AP added to Ca2+-free ASW induced only a long-lasting depolarizing plateau. In radial fibres, the action potential duration was slightly increased in the presence of TEA+; it was unaffected by 4AP. In Ca2+-free ASW, TEA+ and 4AP induced an oscillating membrane response which appeared to be dependent on the intensity of the injected current pulse. 7. It is concluded that (a) there are significant differences between the action potentials of longitudinal and radial muscle fibres but that both are dependent on Na+ and Ca2+, (b) in longitudinal fibres, a Ca2+-activated K+ conductance and a TEA+-sensitive voltage-activated K+ conductance contribute to the repolarizing phase of the action potential, the former being predominant, (c) in radial fibres, the repolarizing phase of action potentials probably involves different membrane K+ conductances among which is a TEA+-sensitive K+ conductance.

Calcium Action Potentials in the Skeletal Muscle Fibres of the Stick Insect Carausius Morosus

1981 ◽  
Vol 93 (1) ◽  
pp. 257-267 ◽  
Author(s):  
FRANCES M. ASHCROFT
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Inhibitory Effect ◽  
Stick Insect ◽  
Muscle Fibres ◽  
Carausius Morosus ◽  
Outward Currents ◽  
Ca Antagonist ◽  
Ventral Longitudinal Muscle ◽  
Skeletal Muscle Fibres

The ionic requirements for the generation of action potentials in the ventral longitudinal muscle fibres of the stick insect, Carausius morosus, were investigated. Ca-free Ringer rapidly and reversibly abolished the action potential. In the presence of tetraethylammonium (TEA) ions (to suppress outward currents) the overshoot of the action potential changed 26 mV for a 10-fold change in [Ca]o. The maximum rate of rise of the action potential (measured in TEA Ringer) showed saturation at high [Ca]o. Cobaltous ions (20 mM) and the organic Ca antagonist D 600 (5×10−4g/ml) reversibly inhibited the action potential; the inhibitory effect of 1 mM-La3+ was irreversible. Barium and strontium, but not magnesium, were able to substitute for calcium as charge carriers. These results suggest that an inward movement of Ca2+ underlies the action potential of Carausius fibres.

scholarly journals The Effect of Aconitine on the Giant Axon of the Squid

1964 ◽  
Vol 47 (4) ◽  
pp. 719-733 ◽  
Author(s):  
W. H. Herzog ◽  
R. M. Feibel ◽  
S. H. Bryant
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Giant Axon ◽  
Membrane Resistance ◽  
Repetitive Stimulation ◽  
Resting Membrane Potential ◽  
Sustained Activity ◽  
Frequency Of Stimulation ◽  
Sodium And Potassium

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.

scholarly journals Acidosis facilitates spontaneous sarcoplasmic reticulum Ca2+ release in rat myocardium.

1987 ◽  
Vol 90 (1) ◽  
pp. 145-165 ◽  
Author(s):  
C H Orchard ◽  
S R Houser ◽  
A A Kort ◽  
A Bahinski ◽  
M C Capogrossi ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potentials ◽  
Laser Light ◽  
De Novo ◽  
Resting Membrane Potential ◽  
Resting Tension ◽  
Spontaneous Action ◽  
The Mean ◽  
Spontaneous Action Potentials ◽  
Tissue Motion

Previous studies have shown that acidosis increases myoplasmic [Ca2+] (Cai). We have investigated whether this facilitates spontaneous sarcoplasmic reticulum (SR) Ca2+ release and its functional sequelae. In unstimulated rat papillary muscles, exposure to an acid solution (produced by increasing the [CO2] of the perfusate from 5 to 20%) caused a rapid increase in the mean tissue Cai, as measured by the photoprotein aequorin. This was paralleled by an increase in spontaneous microscopic tissue motion caused by localized Ca2+ myofilament interactions, as monitored in fluctuations in the intensity of laser light scattered by the muscle. In regularly stimulated muscles, acidosis increased the size of the Ca2+ transient associated with each contraction and caused the appearance of Cai oscillations in the diastolic period. In unstimulated single myocytes, acidosis depolarized the resting membrane potential by approximately 5 mV and enhanced the frequency of spontaneous contractile waves. The small sarcolemmal depolarization associated with each contractile wave increased and occasionally initiated spontaneous action potentials. In regularly stimulated myocytes, acidosis caused de novo spontaneous contractile waves between twitches; these waves were associated with a decrease in the amplitude of the subsequent stimulated twitch. Ryanodine (2 microM) abolished all evidence of spontaneous Ca2+ release during acidosis, markedly reduced the acidosis-induced increase in aequorin light, and reduced resting tension. We conclude that acidosis increases the likelihood for the occurrence of spontaneous SR Ca2+ release, which can cause spontaneous action potentials, increase resting tension, and negatively affect twitch tension.

Changes in cytosolic calcium monitored by inward currents during action potentials in guinea-pig ventricular cells

1989 ◽  
Vol 238 (1291) ◽  
pp. 171-188 ◽  
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Voltage Clamp ◽  
Action Potentials ◽  
Single Cells ◽  
Calcium Transient ◽  
Cytosolic Calcium ◽  
Time To Peak ◽  
Ventricular Cells ◽  
In Cells

Action potentials were recorded from single cells isolated from guinea-pig ventricular muscle. Contraction was measured with an optical technique. Tail currents thought to be activated by cytosolic calcium were recorded when action potentials were interrupted by application of a voltage-clamp. A family of tail currents was recorded by interrupting the action potential at various times after the upstroke. The envelope of tail current amplitudes was taken as an index of changes in cytosoli calcium. Con­sistent with this interpretation, tail currents were negligible following intracellular loading with the calcium chelator BAPTA to suppress calcium transients. The cytosolic calcium transient estimated from the envelope of tails reached a peak approximately 50 ms after the upstroke of the action potential, and fell close to diastolic levels before repolarization was com­plete; 10 mM caffeine delayed the time to peak contraction, and caused a prolongation of the cytosolic calcium transient estimated from the envelope of tail currents. Caffeine also induced the appearance of a distinct late plateau phase of the action potential. Intracellular BAPTA suppressed the late plateau, contraction and tail currents in cells exposed to caffeine. Exposure to caffeine increased the time constant for decay of tail currents (from approximately 35 to 70 ms). When action potentials were greatly abbreviated by interruption with a voltage-clamp, a pro­gressive decline occurred in the subsequent three contractions and tail currents. There was a progressive reversal of these effects over four responses when the full action potential duration was restored. None of these effects was observed in cells exposed to caffeine. Calcium-activated tail currents appear to be a useful qualitative index of changes in cytosolic calcium. The observations are consistent with the suggestion that cytosolic calcium is reduced during the plateau by a combination of calcium extrusion through Na–Ca exchange and calcium uptake into caffeine-sensitive stores. It also appears that reduction of stores loading during abbreviated action potentials reduces subsequent contraction in cells not exposed to caffeine.

scholarly journals Imaging action potential in single mammalian neurons by tracking the accompanying sub-nanometer mechanical motion

2017 ◽  
Author(s):  
Yunze Yang ◽  
Xian-Wei Liu ◽  
Hui Yu ◽  
Yan Guan ◽  
Shaopeng Wang ◽  
...  
Keyword(s):  
Detection Limit ◽  
Patch Clamp ◽  
Action Potential ◽  
Fluorescence Detection ◽  
Action Potentials ◽  
Single Cells ◽  
Detection Methods ◽  
Imaging Method ◽  
Label Free ◽  
Mechanical Motion

AbstractAction potentials in neurons have been studied traditionally by the patch clamp and more recently by the fluorescence detection methods. Here we describe a label-free optical imaging method that can measure mechanical motion in single cells with sub-nanometer detection limit and sub-millisecond temporal resolution. Using the method, we have observed sub-nanometer mechanical motion accompanying the action potential in single mammalian neurons. The shape and width of the transient displacement are similar to those of the electrically recorded action potential, but the amplitude varies from neuron to neuron, and from one region of a neuron to another, ranging from 0.2 - 0.4 nm. The work indicates that action potentials may be studied non-invasively in single mammalian neurons by label-free imaging of the accompanying subnanometer mechanical motion.

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