scholarly journals Voltage-Activated Potassium Outward Currents in Two Types of Spider Mechanoreceptor Neurons

1999 ◽  
Vol 81 (6) ◽  
pp. 2937-2944 ◽  
Author(s):  
Shin-Ichi Sekizawa ◽  
Andrew S. French ◽  
Ulli Höger ◽  
Päivi H. Torkkeli
Keyword(s):  
Outward Current ◽  
Type A ◽  
Transient Current ◽  
Resting Potential ◽  
Transient Outward Current ◽  
Type B ◽  
Outward Currents ◽  
The Difference ◽  
Major Factors ◽  
Kinetics Of

Voltage-activated potassium outward currents in two types of spider mechanoreceptor neurons. We studied the properties of voltage-activated outward currents in two types of spider cuticular mechanoreceptor neurons to learn if these currents contribute to the differences in their adaptation properties. Both types of neurons adapt rapidly to sustained stimuli, but type A neurons usually only fire one or two action potentials, whereas type B neurons can fire bursts lasting several hundred milliseconds. We found that both neurons had two outward current components, 1) a transient current that activated rapidly when stimulated from resting potential and inactivated with maintained stimuli and 2) a noninactivating outward current. The transient outward current could be blocked by 5 mM tetraethylammonium chloride, 5 mM 4-aminopyridine, or 100 μM quinidine, but these blockers also reduced the amplitude of the noninactivating outward current. Charybdotoxin or apamin did not have any effect on the outward currents, indicating that Ca2+-activated K+ currents were not present or not inhibited by these toxins. The only significant differences between type A and type B neurons were found in the half-maximal activation ( V 50) values of both currents. The transient current had a V 50 value of 9.6 mV in type A neurons and −13.1 mV in type B neurons, whereas the V 50 values of noninactivating outward currents were −48.9 mV for type A neurons and −56.7 mV for type B neurons. We conclude that, although differences in the activation kinetics of the voltage-activated K+ currents could contribute to the difference in the adaptation behavior of type A and type B neurons, they are not major factors.

Transient outward current in young and adult diseased human atria

1993 ◽  
Vol 265 (4) ◽  
pp. H1466-H1470 ◽  
Author(s):  
J. Mansourati ◽  
B. Le Grand
Keyword(s):  
Action Potential ◽  
Developmental Change ◽  
Single Cells ◽  
Young Patients ◽  
Outward Current ◽  
Cell Voltage ◽  
Transient Outward Current ◽  
Normal Cells ◽  
Outward Currents ◽  
The Difference

In human atrial fibers, the action potential undergoes a major developmental change in shape in the months immediately after birth. Transient potassium outward currents, which may affect the shape of the action potential, have been studied using a whole cell voltage-clamp technique with single cells from the atria of young patients aged 3-60 mo. Transient outward current (I(to)) amplitude was measured as the difference between the peak current and the steady-state outward current (I(late)) at the end of the voltage step. The density of I(to) was significantly reduced in adult diseased cells (n = 18) compared with normal cells (n = 21) in a large range of potential and absent in young diseased cells (n = 13). Furthermore, the I(late) recorded in young cells was significantly greater (23.7 +/- 5.74 pA/pF at 60 mV) than in adult normal cells (12.71 +/- 2.25 pA/pF at 60 mV), whereas I(late) was not significantly different between both groups of adult cells. Nevertheless, a 4-aminopyridine-sensitive I(to) has been recorded in young cells. A decrease in the frequency of clamp steps (from 0.1 to 0.01 Hz) did not reactivate a I(to) in young cells. This absence of 4-aminopyridine-sensitive Ito in young cells probably results from either a normal developmental change of this current or from pathological alterations like those described in adult diseased atria.

Slow inactivation of a TEA-sensitive K current in acutely isolated rat thalamic relay neurons

1991 ◽  
Vol 66 (4) ◽  
pp. 1316-1328 ◽  
Author(s):  
J. R. Huguenard ◽  
D. A. Prince
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Outward Current ◽  
Resting Potential ◽  
Transient Outward Current ◽  
Voltage Range ◽  
Voltage Dependent ◽  
Kinetics Of ◽  
K Currents ◽  
Relay Neurons

1. Voltage-gated K currents were studied in relay neurons (RNs) acutely isolated from somatosensory (VB) thalamus of 7- to 14-day-old rats. In addition to a rapidly activated, transient outward current, IA, depolarizations activated slower K+ currents, which were isolated through the use of appropriate ionic and pharmacological conditions and measured via whole-cell voltage-clamp. 2. At least two slow components of outward current were observed, both of which were sensitive to changes in [K+]o, as expected for K conductances. The first, IK1, had an amplitude that was insensitive to holding potential and a relatively small conductance of 150 pS/pF. It was blocked by submillimolar levels of tetraethylammonium [TEA, 50%-inhibitory concentration (IC50 = 30 microM)] and 4-aminopyridine (4-AP, 40 microM). In the absence of intracellular Ca2+ buffering, the amplitude of IK1 was both larger and dependent on holding potential, as expected for a Ca(2+)-dependent current. Replacement of [Ca2+]o by Co2+ reduced IK1, although the addition of Cd2+ to Ca(2+)-containing solutions had no effect. 3. The second component, IK2, had a normalized conductance of 2.0 nS/pF and was blocked by millimolar concentrations of TEA (IC50 = 4 mM) but not by 4AP. The kinetics of IK2 were analogous to (but much slower than) those of IA in that both currents displayed voltage-dependent activation and voltage-independent inactivation. IK2 was not reduced by the addition of Cd2+ to Ca(2+)-containing solutions or by replacement of Ca2+ by Co2+. 4. IK2 had a more depolarized activation threshold than IA and attained peak amplitude with a latency of approximately 100 ms at room temperature. IK2 decay was nonexponential and could be described as the sum of two components with time constants (tau) near 1 and 10 s. 5. IK2 was one-half steady-state inactivated at a membrane potential of -63 mV, near the normal resting potential for these cells. The slope factor of the Boltzman function describing steady-state inactivation was 13 mV-1, which indicates that IK2 varies in availability across a broad voltage range between -100 and -20 mV. 6. Activation kinetics of IK2 were voltage dependent, with peak latency shifting from 300 to 50 ms in the voltage range -50 to +30 mV. Deinactivation and deactivation were also voltage dependent, in contrast to inactivation, which showed little dependence on membrane potential. Increase in temperature sped the kinetics of IK2, with temperature coefficient (Q10) values near 3 for activation and inactivation. Heating increased the amplitude of IK2 with a Q10 value near 2.(ABSTRACT TRUNCATED AT 400 WORDS)

Differences in outward currents between neonatal and adult rabbit ventricular cells

1994 ◽  
Vol 266 (3) ◽  
pp. H1184-H1194 ◽  
Author(s):  
J. Sanchez-Chapula ◽  
A. Elizalde ◽  
R. Navarro-Polanco ◽  
H. Barajas
Keyword(s):  
Action Potential ◽  
Papillary Muscle ◽  
Action Potential Duration ◽  
Outward Current ◽  
Stimulation Frequency ◽  
Transient Outward Current ◽  
Adult Rabbit ◽  
Outward Currents ◽  
Recovery From Inactivation ◽  
In Cells

In adult rabbit ventricular preparations, action potential duration is significantly increased when stimulation frequency is increased from 0.1 to 1.0 Hz. In neonatal preparations, a similar change in stimulation frequency produced no significant increase in action potential duration. To identify the ionic basis for this difference, we studied different outward currents in single myocytes from papillary muscle and from epicardial tissue of adult and neonatal rabbits. The densities of the outward currents in neonatal cells were about one-half of the current density in adult cells. The density of the voltage-activated transient outward current (I(to1)) was smaller in cells from papillary muscle than in cells from epicardium in adult and newborn rabbits. We found major differences in the kinetic behavior of I(to1) between adult and neonatal cells: 1) the rate of apparent inactivation was faster in neonatal cells, and 2) the recovery from inactivation was significantly faster in neonatal cells, with a time constant of 113 vs. 1,356 ms. We propose that this marked difference in the recovery from inactivation of I(to1) is the basis for the difference in frequency dependence of action potential duration.

Existence of a transient outward K+ current in guinea pig cardiac myocytes

2000 ◽  
Vol 279 (1) ◽  
pp. H130-H138 ◽  
Author(s):  
Gui-Rong Li ◽  
Baofeng Yang ◽  
Haiying Sun ◽  
Clive M. Baumgarten
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Resting Potential ◽  
Transient Outward Current ◽  
Time Constants ◽  
Zero Current ◽  
Steady State Inactivation ◽  
K Current ◽  
External K

A novel transient outward K+current that exhibits inward-going rectification ( I to.ir) was identified in guinea pig atrial and ventricular myocytes. I to.ir was insensitive to 4-aminopyridine (4-AP) but was blocked by 200 μmol/l Ba2+or removal of external K+. The zero current potential shifted 51–53 mV/decade change in external K+. I to.ir density was twofold greater in ventricular than in atrial myocytes, and biexponential inactivation occurs in both types of myocytes. At −20 mV, the fast inactivation time constants were 7.7 ± 1.8 and 6.1 ± 1.2 ms and the slow inactivation time constants were 85.1 ± 14.8 and 77.3 ± 10.4 ms in ventricular and atrial cells, respectively. The midpoints for steady-state inactivation were −36.4 ± 0.3 and −51.6 ± 0.4 mV, and recovery from inactivation was rapid near the resting potential (time constants = 7.9 ± 1.9 and 8.8 ± 2.1 ms, respectively). I to.ir was detected in Na+-containing and Na+-free solutions and was not blocked by 20 nmol/l saxitoxin. Action potential clamp revealed that I to.ir contributed an outward current that activated rapidly on depolarization and inactivated by early phase 2 in both tissues. Although it is well known that 4-AP-sensitive transient outward current is absent in guinea pig, this Ba2+-sensitive and 4-AP-insensitive K+ current has been overlooked.

Transient voltage and calcium-dependent outward currents in hippocampal CA3 pyramidal neurons

1985 ◽  
Vol 53 (4) ◽  
pp. 1038-1058 ◽  
Author(s):  
K. L. Zbicz ◽  
F. F. Weight
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Sympathetic Neurons ◽  
Outward Current ◽  
Transient Current ◽  
Transient Outward Current ◽  
Molluscan Neurons ◽  
Voltage Sensitivity ◽  
Transient Currents ◽  
Fast Transient

Membrane currents activated by step changes in membrane potential were studied in hippocampal pyramidal neurons of region CA3 using the single microelectrode voltage-clamp technique. The transient outward current activated by depolarizing steps appeared to be composed of two transient currents that could be distinguished by differences in voltage sensitivity, time course, and pharmacological sensitivity. The more slowly decaying current was activated by voltage steps positive to -60 mV and declined exponentially with a time constant between 200 and 400 ms. This current inactivated as the holding potential was made more positive over the range of -75 to -45 mV and was 50% inactivated near -60 mV. The more slowly decaying transient current was selectively blocked by 0.5 mM 4-aminopyridine (4-AP) but not by 5-10 mM tetraethylammonium (TEA) or 2-5 mM Mn2+. The second transient current had a much faster time course than the 4-AP-sensitive current, having a duration of 5-20 ms. This very fast transient current was observed during potential steps positive to -45 mV. The fast transient current was inactivated when the holding potential was made positive to -45 mV. The amplitude of the fast transient current was greatly reduced by the application of 4 mM Mn2+ or Ca2+-free artificial cerebrospinal fluid (CSF). The fast transient current appeared to be unaffected by 0.5 mM 4-AP but was greatly reduced by 10 mM TEA. These results suggest that the transient outward current observed during depolarizing steps is composed of at least two distinct transient currents. The more slowly decaying current resembles the A-current originally described in molluscan neurons (9, 32, 42) in voltage sensitivity, time course, and pharmacological sensitivity. The faster transient current resembles a fast, Ca2+-dependent transient current previously observed in bull-frog sympathetic neurons (5, 27).

Transient potassium currents in avian sensory neurons

1990 ◽  
Vol 63 (4) ◽  
pp. 725-737 ◽  
Author(s):  
S. K. Florio ◽  
C. D. Westbrook ◽  
M. R. Vasko ◽  
R. J. Bauer ◽  
J. L. Kenyon
Keyword(s):  
Single Channel ◽  
Outward Current ◽  
Potassium Currents ◽  
Delayed Rectifier ◽  
Transient Outward Current ◽  
Single Channels ◽  
Patch Clamp Technique ◽  
Small Component ◽  
Whole Cell ◽  
Outward Currents

1. We used the patch-clamp technique to study voltage-activated transient potassium currents in freshly dispersed and cultured chick dorsal root ganglion (DRG) cells. Whole-cell and cell-attached patch currents were recorded under conditions appropriate for recording potassium currents. 2. In whole-cell experiments, 100-ms depolarizations from normal resting potentials (-50 to -70 mV) elicited sustained outward currents that inactivated over a time scale of seconds. We attribute this behavior to a component of delayed rectifier current. After conditioning hyperpolarizations to potentials negative to -80 mV, depolarizations elicited transient outward current components that inactivated with time constants in the range of 8-26 ms. We attribute this behavior to a transient outward current component. 3. Conditioning hyperpolarizations increased the rate of activation of the net outward current implying that the removal of inactivation of the transient outward current allows it to contribute to early outward current during depolarizations from negative potentials. 4. Transient current was more prominent on the day the cells were dispersed and decreased with time in culture. 5. In cell-attached patches, single channels mediating outward currents were observed that were inactive at resting potentials but were active transiently during depolarizations to potentials positive to -30 mV. The probability of channels being open increased rapidly (peaking within approximately 6 ms) and then declined with a time constant in the range of 13-30 ms. With sodium as the main extracellular cation, single-channel conductances ranged from 18 to 32 pS. With potassium as the main extracellular cation, the single-channel conductance was approximately 43 pS, and the channel current reversed near 0 mV, as expected for a potassium current. 6. We conclude that the transient potassium channels mediate the component of transient outward current seen in the whole-cell experiments. This current is a relatively small component of the net current during depolarizations from normal resting potentials, but it can contribute significant outward current early in depolarizations from hyperpolarized potentials.

Potassium currents and membrane excitability of neurons in the rat's dorsal nucleus of the lateral lemniscus

1996 ◽  
Vol 76 (2) ◽  
pp. 1121-1132 ◽  
Author(s):  
X. W. Fu ◽  
S. H. Wu ◽  
B. L. Brezden ◽  
J. B. Kelly
Keyword(s):  
Cell Membrane ◽  
Time Constant ◽  
Action Potentials ◽  
Outward Current ◽  
Independent Component ◽  
Transient Current ◽  
Transient Outward Current ◽  
Membrane Excitability ◽  
Dorsal Nucleus ◽  
Excitability Of Neurons

1. The contribution of voltage-activated outward potassium currents to membrane excitability of neurons in the rat's dorsal nucleus of the lateral lemniscus (DNLL) was studied in a brain slice preparation using whole cell patch-clamp and intracellular recordings. Voltage-clamp methods and pharmacological manipulations were used to examine the currents regulating membrane dynamics in DNLL. 2. A delayed sustained outward current was evoked by applying depolarizing voltage steps across the cell membrane from a holding potential of -50 mV. An additional transient outward current was evoked when the depolarizing steps were preceded by a hyperpolarizing prepulse of -110 or -120 mV. 3. The transient outward current peaked within 6.8 ms of the onset of a depolarizing pulse. It decayed with a time constant of 12.3 ms for a 60-mV depolarizing voltage shift. Half-inactivation of this current occurred at -81.3 mV. The time constant for removal of the inactivation was 17.4 ms. The transient current had a high sensitivity to 4-aminopyridine (4-AP). 4. The sustained current was activated more slowly and was more sensitive to tetraethylammonium (TEA) than the transient current. The sustained current had both Ca2+-dependent and Ca2+-independent components. The Ca2+-dependent portion emerged at potentials of about -35 mV and was activated fully at +10 mV. The Ca2+-independent component was activated at potentials more positive than -40 mV and increased in magnitude with further depolarization. Inactivation of the Ca2+-independent component was voltage dependent. Also, TEA suppressed the Ca2+-independent compound. 5. The transient current in DNLL neurons closely resembled the A current (IA) described for hippocampal and other neurons in both kinetics and pharmacology. The Ca2+-independent component of the sustained current resembled the K current (IK) described for other neurons in both its properties of activation and inactivation and its pharmacology. 6. The outward current of some DNLL neurons was found to contain a dendrotoxin-sensitive component. This component reached its peak at 6.8 ms and had voltage-sensitive time constants of decay of 25.5 and 8.5 ms with voltage steps of 40 and 60 mV, respectively. 7. Application of 4-AP and TEA markedly prolonged the spike width, abolished the fast component of the after hyperpolarization and depolarized the cell membrane. Also, the number of action potentials produced by positive current injection increased under the influence of 4-AP and TEA. Membrane excitability and spike repolarization were dependent on both 4-AP-sensitive transient and TEA-sensitive sustained currents. 8. Neurons in DNLL typically exhibit a steady discharge of action potentials in response to sustained membrane depolarization. The rate and temporal pattern of production of action potentials in these cells are determined by the combination of transient and sustained potassium channels.

scholarly journals MicroRNA-210 Mediates Hypoxia-Induced Repression of Spontaneous Transient Outward Currents in Sheep Uterine Arteries During Gestation

Hypertension ◽  
2021 ◽  
Vol 77 (4) ◽  
pp. 1412-1427
Author(s):  
Xiang-Qun Hu ◽  
Chiranjib Dasgupta ◽  
Rui Song ◽  
Monica Romero ◽  
Sean M. Wilson ◽  
...  
Keyword(s):  
High Altitude ◽  
Intrauterine Growth Restriction ◽  
Hormonal Regulation ◽  
Outward Current ◽  
Transient Outward Current ◽  
Uterine Arteries ◽  
Outward Currents ◽  
Low Altitude ◽  
Spontaneous Transient Outward Currents

Hypoxia during pregnancy is a major contributor to the pathogenesis of preeclampsia and intrauterine growth restriction. Our recent studies revealed that pregnancy-induced uterine vascular adaptation depended on the enhanced Ca 2+ spark/spontaneous transient outward current (STOC) coupling and hypoxia during gestation diminished this adaption. In the present study, we test the hypothesis of a mechanistic link of microRNA-210 (miR-210) in hypoxia-impaired Ca 2+ spark/STOC coupling in uterine arteries. Pregnant ewes acclimatized to high-altitude (3801 m) hypoxia for ≈110 days significantly increased circulation levels of miR-210 in both the ewe and her fetus. Treatment of uterine arteries from high-altitude animals with the antagomir miR-210-LNA recovered hypoxia-repressed STOCs in pregnant ewes and restored the hormonal regulation of STOCs in nonpregnant animals. In uterine arteries from low-altitude control animals, miR-210 mimic suppressed STOCs in pregnant ewes and inhibited the hormonal regulation of STOCs in nonpregnant animals. Mechanistically, miR-210 directly targeted and downregulated type 2 ryanodine receptor and large-conductance Ca 2+ -activated K + channel β1 subunit, resulting in significant decreases in Ca 2+ sparks and STOCs in uterine arteries. In addition, miR-210 indirectly decreased STOCs by targeting ten-eleven translocation methylcytosine dioxygenase. Together, the present study revealed a mechanistic link of miR-210 in hypoxia-induced repression of Ca 2+ spark/STOC coupling in uterine arteries during gestation, providing novel insights into the understanding of pregnancy complications associated with hypoxia and the potential therapeutic targets.

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)

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