Time course of postnatal changes in rat heart action potential and in transient outward current is different

1994 ◽  
Vol 267 (3) ◽  
pp. H1157-H1166 ◽  
Author(s):  
G. M. Wahler ◽  
S. J. Dollinger ◽  
J. M. Smith ◽  
K. L. Flemal
Keyword(s):  
Action Potential ◽  
Rat Heart ◽  
Action Potentials ◽  
Time Course ◽  
Outward Current ◽  
Transient Outward Current ◽  
Papillary Muscles ◽  
Isolated Cells ◽  
Time Courses ◽  
Action Potential Shortening

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito. In 8- to 10-day muscles, 4-AP caused a small, but significant, increase in APD25. Ito increased slightly between day 1 and days 8-10, but this increase was not significant. Most of the increase in Ito (79%) and in the response to 4-AP (64%) occurred between days 8-10 and adult; however, approximately 75% of the APD25 shortening took place by days 8-10. Thus, while Ito may contribute to repolarization in late neonatal and adult cells, the different time courses of action potential shortening and increases in Ito suggest that changes in Ito are unlikely to be responsible for most of the postnatal action potential shortening.

Outward current and repolarization in hypoxic rat myocardium

1983 ◽  
Vol 244 (3) ◽  
pp. H341-H350
Author(s):  
C. H. Conrad ◽  
R. G. Mark ◽  
O. H. Bing
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Outward Current ◽  
Iodoacetic Acid ◽  
Mechanical Activity ◽  
Potential Range ◽  
Papillary Muscles ◽  
Rat Myocardium ◽  
Cable Properties ◽  
Sucrose Gap

We studied the effects of brief periods (20-30 min) of hypoxia in the presence of 5 and 50 mM glucose and of glycolytic blockade (10(-4) M iodoacetic acid, IAA) on action potentials, membrane currents, and mechanical activity in rat ventricular papillary muscles using a single sucrose gap voltage-clamp technique. Steady-state outward current (iss) was determined at the end of a 500-ms clamp to the test potential following a 600-ms clamp to a holding potential of -50 mV. In the presence of 5 mM glucose, hypoxia resulted in a decrease in action potential duration (APD) and an increase in iss (on the order of 60% at 0 mV) over the potential range studied. The increase in iss did not appear to be due to an increase in leakage current or to a change in the cable properties of the preparation. Addition of 50 mM glucose prevented the change in both APD and iss with hypoxia. In addition, glycolytic blockade with IAA did not alter iss in the presence of oxygen. We conclude that an increase in iss appears to be a major factor in the abbreviation of rat ventricular action potential seen with hypoxia. Glycolysis appears to be a sufficient (with 50 mM glucose) but not necessary source of energy for the maintenance of normal iss.

Electrophysiological properties of neurons within the nucleus ambiguus of adult guinea pigs

1991 ◽  
Vol 66 (3) ◽  
pp. 744-761 ◽  
Author(s):  
S. M. Johnson ◽  
P. A. Getting
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Outward Current ◽  
Nucleus Ambiguus ◽  
Transient Outward Current ◽  
Maximum Magnitude ◽  
Action Potential Firing ◽  
Onset Of Action ◽  
Electrophysiological Properties ◽  
Single Action

1. The purpose of this study was to determine the electrophysiological properties of neurons within the region of the nucleus ambiguus (NA), an area that contains the ventral respiratory group. By the use of an in vitro brain stem slice preparation, intracellular recordings from neurons in this region (to be referred to as NA neurons, n = 235) revealed the following properties: postinhibitory rebound (PIR), delayed excitation (DE), adaptation, and posttetanic hyperpolarization (PTH). NA neurons were separated into three groups on the basis of their expression of PIR and DE: PIR cells (58%), DE cells (31%), and Non cells (10%). Non cells expressed neither PIR nor DE and no cells expressed both PIR and DE. 2. PIR was a transient depolarization that produced a single action potential or a burst of action potentials when the cell was released from hyperpolarization. In the presence of tetrodotoxin (TTX), the maximum magnitude of PIR was 7-12 mV. Under voltage-clamp conditions, hyperpolarizing voltage steps elicited a small inward current during the hyperpolarization and a small inward tail current on release from hyperpolarization. These currents, which mediate PIR, were most likely due to Q-current because they were blocked with extracellular cesium and were insensitive to barium. 3. DE was a delay in the onset of action potential firing when cells were hyperpolarized before application of depolarizing current. When cells were hyperpolarized to -90 mV for greater than or equal to 300 ms, maximum delays ranged from 150 to 450 ms. The transient outward current underlying DE was presumed to be A-current because of the current's activation and inactivation characteristics and its elimination by 4-aminopyridine (4-AP). 4. Adaptation was examined by applying depolarizing current for 2.0 s and measuring the frequency of evoked action potentials. Although there was a large degree of variability in the degree of adaptation, PIR cells tended to express less adaptation than DE and Non cells. Nearly three-fourths of all NA neurons adapted rapidly (i.e., 50% adaptation in less than 200 ms), but PIR cells tended to adapt faster than DE and Non cells. PTH after a train of action potentials was relatively rare and occurred more often in DE cells (43%) and Non cells (33%) than in PIR cells (13%). PTH had a magnitude of up to 18 mV and time constants that reflected the presence of one (1.7 +/- 1.4 s, mean +/- SD) or two components (0.28 +/- 0.13 and 4.1 +/- 2.2 s).(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Properties of tetraethylammonium ion-resistant K+ channels in the photoreceptor membrane of the giant barnacle.

1981 ◽  
Vol 77 (6) ◽  
pp. 629-646 ◽  
Author(s):  
D R Edgington ◽  
A E Stuart
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Cardiac Glycosides ◽  
Time Course ◽  
Photoreceptor Membrane ◽  
K Channels ◽  
Na Pump ◽  
Tetraethylammonium Ion ◽  
Electrogenic Na Pump ◽  
Time Courses

After the offset of illumination, barnacle photoreceptors undergo a large hyperpolarization that lasts seconds or minutes. We studied the mechanisms that generate this afterpotential by recording afterpotentials intracellularly from the medial photoreceptors of the giant barnacle Balanus nubilus. The afterpotential has two components with different time-courses: (a) an earlier component due to an increase in conductance to K+ that is not blocked by extracellular tetraethylammonium ion (TEA+) or 3-aminopyridine (3-AP) and (b) a later component that is sensitive to cardiac glycosides and that requires extracellular K+, suggesting that it is due to an electrogenic Na+ pump. The K+ conductance component increases in amplitude with increasing CA++ concentration and is inhibited by extracellular Co++; the Co++ inhibition can be overcome by increasing the Ca++ concentration. Thus, the K+ conductance component is Ca++ dependent. An afterpotential similar to that evoked by a brief flash of light is generated by depolarization with current in the dark and by eliciting Ca++ action potentials in the presence of TEA+ in the soma, axon, or terminal regions of the photoreceptor. The action potential undershoot is generated by an increase in conductance to K+ that is resistant to TEA+ and 3-AP and inhibited by Co++. The similarity in time-course and pharmacology of the hyperpolarization afterpotentials elicited by (a) a brief flash of light, (b) depolarization with current, and (c) an action potential indicates that Ca++-dependent K+ channels throughout the photoreceptor membrane are responsible for all three hyperpolarizing events.

Effects of myocardial hypertrophy on transient outward current

1994 ◽  
Vol 266 (5) ◽  
pp. H1738-H1745 ◽  
Author(s):  
Q. Li ◽  
E. C. Keung
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Action Potential Duration ◽  
Time Course ◽  
Myocardial Hypertrophy ◽  
Pressure Overload ◽  
Reversal Potential ◽  
Outward Current ◽  
Transient Outward Current ◽  
The Difference

In the one-clip, two-kidney model of hypertensive rat, a gradual chronic pressure overload is imposed on the heart. Myocardial hypertrophy resulting from such pressure overload is associated with an increased but slower inactivating L-type calcium current and prolongation of action potential duration. Voltage clamp experiments in a variety of excitable tissues indicate that a 4-aminopyridine-sensitive transient outward current (Ito) plays an important role in regulating the action potential duration. Accordingly, we studied Ito in single adult cardiac myocytes enzymatically isolated from hypertrophied left ventricles of the renovascular hypertensive (HBP) rat hearts using the whole cell patch-clamp method. The current densities (normalized to cell capacitative surface area) measured at the early transient peak Ito, at the steady state, and as the difference between the transient peak and the steady state were larger in HBP cells (n = 23) than in control (Ctrl) cells (n = 20) (P < 0.05). There was no difference in the Ito reversal potential between Ctrl (-60.9 +/- 1.9 mV, mean +/- SE; n = 16) and HBP (-63.7 +/- 2.6 mV; n = 19) cells. The observed increase in Ito amplitude was not due to an increase in the number of channels available for activation or in the fraction of channels activated because there were no statistical differences in the membrane potential at which one-half of the Ito channels are activated (V0.5) for the steady-state activation and inactivation curves between Ctrl and HBP cells. The time course of inactivation of Ito was described by a double-exponential function.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Diverse Ionic Currents and Electrical Activity of Cultured Myenteric Neurons From the Guinea Pig Proximal Colon

2000 ◽  
Vol 83 (3) ◽  
pp. 1253-1263 ◽  
Author(s):  
Fivos Vogalis ◽  
Kirk Hillsley ◽  
Terence K. Smith
Keyword(s):  
Patch Clamp ◽  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Outward Current ◽  
Proximal Colon ◽  
Equilibrium Potential ◽  
Transient Outward Current ◽  
Myenteric Neurons ◽  
Fast Transient

The aim of this study was to perform a patch-clamp analysis of myenteric neurons from the guinea pig proximal colon. Neurons were enzymatically dispersed, cultured for 2–7 days, and recorded from using whole cell patch clamp. The majority of cells fired phasically, whereas about one-quarter of the neurons fired in a tonic manner. Neurons were divided into three types based on the currents activated. The majority of tonically firing neurons lacked an A-type current, but generated a large fast transient outward current that was associated with the rapid repolarizing phase of an action potential. The fast transient outward current was dependent on calcium entry and was blocked by tetraethylammonium. Cells that expressed both an A-type current and a fast transient outward current were mostly phasic. Depolarization of these cells to suprathreshold potentials from less than −60 mV failed to trigger action potentials, or action potentials were only triggered after a delay of >50 ms. However, depolarizations from more positive potentials triggered action potentials with minimal latency. Neurons that expressed neither the A-type current or the fast transient outward current were all phasic. Sixteen percent of neurons were similar to AH/type II neurons in that they generated a prolonged afterhyperpolarization following an action potential. The current underlying the prolonged afterhyperpolarization showed weak inward rectification and had a reversal potential near the potassium equilibrium potential. Thus cultured isolated myenteric neurons of the guinea pig proximal colon retain many of the diverse properties of intact neurons. This preparation is suitable for further biophysical and molecular characterization of channels expressed in colonic myenteric neurons.

Ca(2+)-dependent outward currents in myocytes from epicardial border zone of 5-day infarcted canine heart

1997 ◽  
Vol 273 (3) ◽  
pp. H1386-H1394 ◽  
Author(s):  
R. Aggarwal ◽  
J. Pu ◽  
P. A. Boyden
Keyword(s):  
Action Potentials ◽  
Time Course ◽  
Outward Current ◽  
Border Zone ◽  
Disulfonic Acid ◽  
Transient Outward Current ◽  
Canine Heart ◽  
Whole Cell Patch Clamp ◽  
Outward Currents ◽  
Transmembrane Action Potentials

Myocytes from the epicardial border zone (EBZ) of the 5-day infarcted canine heart (IZ) have abnormal transmembrane action potentials, reduced L-type Ca2+ currents (ICa,L) and altered intracellular Ca2+ (Cai) transients compared with those of normal epicardial myocytes (NZ). We hypothesized that altered Cai cycling might be reflected in differences in Cai-dependent outward currents (Ito2). We recorded Ito2 in NZ and IZ using whole cell patch-clamp techniques. Ito2 was defined as the amplitude of the 4-aminopyridine-resistant transient outward current that was blocked by 200 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) or DIDS+ ryanodine (2 microM). Ito2 were present in both NZ and IZ, but peak density was significantly reduced in IZ, particularly at positive plateau voltages. Time course of decay of Ito2 was biexponential and similar in NZ and IZ. A given peak ICa,L was usually associated with a smaller peak Ito2 in IZ. These differences were exaggerated when Ito2 and Cai transients were determined in rapidly paced cells. In summary, myocytes surviving in the EBZ of the infarcted heart have Ito2, yet they are reduced in density and can vary, particularly at fast pacing rates.

Membrane potential oscillations in molluscan “burster” neurones

1979 ◽  
Vol 81 (1) ◽  
pp. 93-112
Author(s):  
R. W. Meech
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Intracellular Ph ◽  
Action Potentials ◽  
Outward Current ◽  
Ionized Calcium ◽  
Isolated Cells ◽  
Potential Oscillations ◽  
Inward Current ◽  
Membrane Potential Oscillations

Membrane potential oscillations can be induced in molluscan neurones under a variety of artificial conditions. In the so-called ‘burster’ neurones oscillations are generated even in isolated cells. A likely mechanism for ‘bursting’ involves the following ionic currents: 1. A transient inward current carried by Na+ and Ca2+. This current is responsible for the upstroke of the action potentials. 2. A delayed outward current carried by K+. This current is voltage-sensitive and is responsible for the downstroke of the action potential during the early part of the burst. It becomes progressively inactivated during the burst. Its amplitude depends on the intracellular pH. 3. A rapidly developing outward current carried by K+ which is inactivated at potentials close to action potential threshold. This current tends to hold the membrane in the hyperpolarized state and is involved in spacing the action potentials. 4. A prolonged inward current which may not inactivate. It is probably carried by both Na+ and Ca2+. This current is responsible for the depolarizing phase of the burst but also contributes to the action potential. 5. A slowly developing outward current, carried by K+. This current appears as a result of a slow increase in intracellular ionized calcium and is responsible for the hyperpolarizing phase of the burst. Note that a transient increase in this current may also contribute to the falling phase of the action potential during the later stages of the burst. It is also sensitive to intracellular pH. One of the more significant features of this system of producing membrane potential oscillations is that the frequency of the bursts depends on the rate at which the intracellular ionized calcium returns to its resting level. This process depends on the metabolic state of the animal which can thereby exert a considerable influence on the electrical activity of burster neurones.

Mathematical models of action potentials in the periphery and center of the rabbit sinoatrial node

2000 ◽  
Vol 279 (1) ◽  
pp. H397-H421 ◽  
Author(s):  
H. Zhang ◽  
A. V. Holden ◽  
I. Kodama ◽  
H. Honjo ◽  
M. Lei ◽  
...  
Keyword(s):  
Action Potential ◽  
Mathematical Models ◽  
Action Potentials ◽  
Phase 1 ◽  
Outward Current ◽  
Transient Outward Current ◽  
Dimensional Model ◽  
Peripheral Cell ◽  
One Dimensional ◽  
Sa Node

Mathematical models of the action potential in the periphery and center of the rabbit sinoatrial (SA) node have been developed on the basis of published experimental data. Simulated action potentials are consistent with those recorded experimentally: the model-generated peripheral action potential has a more negative takeoff potential, faster upstroke, more positive peak value, prominent phase 1 repolarization, greater amplitude, shorter duration, and more negative maximum diastolic potential than the model-generated central action potential. In addition, the model peripheral cell shows faster pacemaking. The models behave qualitatively the same as tissue from the periphery and center of the SA node in response to block of tetrodotoxin-sensitive Na+current, L- and T-type Ca2+ currents, 4-aminopyridine-sensitive transient outward current, rapid and slow delayed rectifying K+ currents, and hyperpolarization-activated current. A one-dimensional model of a string of SA node tissue, incorporating regional heterogeneity, coupled to a string of atrial tissue has been constructed to simulate the behavior of the intact SA node. In the one-dimensional model, the spontaneous action potential initiated in the center propagates to the periphery at ∼0.06 m/s and then into the atrial muscle at 0.62 m/s.

Spermine Mediates Inward Rectification in Potassium Channels of Turtle Retinal Müller Cells

2001 ◽  
Vol 85 (4) ◽  
pp. 1357-1367 ◽  
Author(s):  
Eduardo Solessio ◽  
Kevin Rapp ◽  
Ido Perlman ◽  
Eric M. Lasater
Keyword(s):  
Potassium Channels ◽  
Time Course ◽  
Müller Cells ◽  
Outward Current ◽  
Membrane Properties ◽  
Inward Rectification ◽  
Transient Outward Current ◽  
Muller Cells ◽  
Isolated Cells ◽  
Inward Current

Retinal Müller cells are highly permeable to potassium as a consequence of their intrinsic membrane properties. Therefore these cells are able to play an important role in maintaining potassium homeostasis in the vertebrate retina during light-induced neuronal activity. Polyamines and other factors present in Müller cells have the potential to modulate the rectifying properties of potassium channels and alter the Müller cells capacity to siphon potassium from the extracellular space. In this study, the properties of potassium currents in turtle Müller cells were investigated using whole cell voltage-clamp recordings from isolated cells. Overall, the currents were inwardly rectifying. Depolarization elicited an outward current characterized by a fast transient that slowly recovered to a steady level along a double exponential time course. On hyperpolarization the evoked inward current was characterized by an instantaneous onset (or step) followed by a slowly developing sustained inward current. The kinetics of the time-dependent components (block of the transient outward current and slowly developing inward current) were dependent on holding potential and changes in the intracellular levels of magnesium ions and polyamines. In contrast, the instantaneous inward and the sustained outward currents were ohmic in character and remained relatively unaltered with changes in holding potential and concentration of applied spermine (0.5–2 mM). Our data suggest that cellular regulation in vivo of polyamine levels can differentially alter specific aspects of potassium siphoning by Müller cells in the turtle retina by modulating potassium channel function.

Ito1 dictates behavior of ICl(Ca) during early repolarization of canine ventricle

1997 ◽  
Vol 273 (3) ◽  
pp. H1096-H1106 ◽  
Author(s):  
A. C. Zygmunt ◽  
D. C. Robitelle ◽  
G. T. Eddlestone
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Phase 1 ◽  
Potassium Conductance ◽  
Outward Current ◽  
Direct Result ◽  
Disulfonic Acid ◽  
Early Repolarization

The contributions of the 4-aminopyridine (4-AP)-sensitive transient outward potassium conductance (Ito1) and the calcium-activated chloride conductance (ICl(Ca)] to cardiac action potentials were investigated in canine ventricular myocytes. Action potentials or currents were recorded at 37 degrees C using standard whole cell or amphotericin B perforated-patch-clamp techniques. Inhibition of Ito1 by 1 mM 4-AP prolonged phase 1 repolarization, elevated the action potential notch, and depressed the plateau. Action potential voltage clamp revealed that 4-AP blocked a rapidly decaying outward current during phase 1 without affecting plateau or diastolic currents. These results suggested that depression of the plateau was not a direct result of Ito1 inhibition but followed from delayed phase 1 repolarization. Calcium current (ICa) at the peak of the action potential dome was reduced 60 +/- 4% when the rate of phase 1 repolarization was reduced. ICl(Ca) measured by action potential clamp reversed over the course of the action potential. Chloride fluxes associated with outward and inward components of the 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid-sensitive current were +130 +/- 17 and -184 +/- 20 (pA.ms)/pF, respectively. The effects of selective inhibition of ICl(Ca) on the action potential were dependent on the rate of early repolarization and the prominence of the notch. Inhibition of ICl(Ca) elevated the plateau and slightly abbreviated action potential duration when the notch was prominent. When repolarization was prolonged and the notch was shallow, inhibition of ICl(Ca) elevated the notch and the plateau and abbreviated duration. We have shown that Ito1 and ICl(Ca) contribute to canine ventricular action potentials. The extent of overlap between Ito1 and ICl(Ca) during the action potential is largely determined by the amplitude of Ito1 and the depth of the notch. Regional differences in the density of Ito1, or interventions that moderate phase 1 repolarization by reducing this current, will have considerable effect on the time course of ICa and calcium-dependent conductances.

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