scholarly journals Serotonin differentially modulates two K+ currents in the Retzius cell of the leech

1989 ◽  
Vol 145 (1) ◽  
pp. 403-417
Author(s):  
J. Acosta-Urquidi ◽  
C. L. Sahley ◽  
A. L. Kleinhaus
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Voltage Clamp ◽  
Negative Feedback ◽  
Outward Current ◽  
Current Clamp ◽  
Macrobdella Decora ◽  
Voltage Dependent ◽  
Retzius Cell ◽  
K Currents

The effects of 100 mumol l-1 serotonin (5-HT) were investigated on the Na+- and Ca2+-dependent action potential and distinct K+ currents in the Retzius (R) cells of the hirudinid leeches Macrobdella decora and Hirudo medicinalis by conventional current-clamp and two-microelectrode voltage-clamp techniques. 1. In normal Na+-containing Ringer, 5-HT decreased the duration of the action potential prolonged by 5 mmol l-1 tetraethylammonium (TEA+) chloride. 2. In Na+-free saline containing 25 mumol l-1 TEA+ to block IK, 5-HT reduced the amplitude and duration of Ca2+ spikes evoked by intracellular current injection. 3. Under voltage-clamp, 5-HT enhanced the peak amplitude of an early transient 4-aminopyridine (4-AP)-sensitive, voltage-dependent outward current, termed IA. A small but significant increase in the time constant of inactivation (tau off) of IA was also measured after exposure to 5-HT. 4. 5-HT suppressed the peak and steady-state amplitudes of a delayed TEA+-sensitive, voltage-dependent outward current, termed IK. These results demonstrate differential simultaneous modulation of distinct K+ currents in the Retzius cell of the leech by the endogenous transmitter serotonin. These cells contain and release 5-HT, and are believed to be multifunction neurons implicated in feeding and swimming. This modulation may change the excitable properties of the cell, leading to a negative feedback autoregulation of its transmitter output.

Ca-Induced K+-Outward Current in Paramecium Tetraurelia

1980 ◽  
Vol 88 (1) ◽  
pp. 293-304 ◽  
Author(s):  
YOUKO SATOW ◽  
CHING KUNG
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Outward Current ◽  
Paramecium Tetraurelia ◽  
Ca Channels ◽  
Outward Currents ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
K Current ◽  
K Outward Current

Late K-outward currents upon membrane depolarization were recorded in Paramecium tetraurelia under a voltage clamp. A Ca-induced K-outward component is demonstrated by subtracting the value of the outward current in a pawn A mutant lacking functional Ca-channels (pwA500). The Ca-induced K-outward current activates slowly, reaching a peak after 100 to 1000 ms. The current then remains steady or reaches the steady state after a decline of several seconds. EGTA2- injection experiments show that the Ca-induced K-outward current is dependent on the internal Ca2+ concentration. The current is shown to depend on the voltage-dependent Ca conductance, by study of the leaky pawn A mutant (pwA132), which has a lowered Ca conductance as well as a lowered Ca-induced K-current. The Ca-induced GK is thus indirectly dependent on the voltage. The maximal GK is about 40 nmho/cell at + 7 mV in 4 mM-K+. The Ca-induced K current is sustained throughout the prolonged depolarization and the prolonged ciliary reversal.

Voltage-clamp analysis of the ionic conductances in a leech neuron with a purely calcium-dependent action potential

1987 ◽  
Vol 58 (6) ◽  
pp. 1468-1484 ◽  
Author(s):  
J. Johansen ◽  
J. Yang ◽  
A. L. Kleinhaus
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Time Course ◽  
Outward Current ◽  
Time Constants ◽  
Exponential Time ◽  
Calcium Dependent ◽  
Voltage Dependent ◽  
Ca Currents ◽  
Single Exponential

1. The purely calcium-dependent action potential of the anterior lateral giant (ALG) cell in the leech Haementeria was examined under voltage clamp. 2. Analysis with ion substitutions showed that the ALG cell action potential is generated by only two time- and voltage-dependent conductance systems, an inward Ca-dependent current (ICa) and an outward Ca-dependent K current IK(Ca). 3. The kinetic properties of the inward current were examined both in Cs-loaded neurons with Ca as the current carrier as well as in Ba-containing Ringer solutions with Ba as the current carrier, since Ba effectively blocked all time- and voltage-dependent outward current. 4. During a maintained depolarization, Ba and Ca currents activated with a time constant tau m, they then inactivated with the decay following a single exponential time course with a time constant tau h. The time constants for decay of both Ba and Ca currents were comparable, suggesting that the mechanism of inactivation of ICa in the ALG cell is largely voltage dependent. In the range of potentials from 5 to 45 mV, tau m varied from 8 to 2 ms and tau h varied from 250 to 125 ms. 5. The activation of currents carried by Ba, after correction for inactivation, could be described reasonably well by the expression I'Ba = I'Ba(infinity) [1--exp(-t/tau m)]. 6. The steady-state activation of the Ba-conductance mBa(infinity) increased sigmoidally with voltage and was approximated by the equation mBa(infinity) = (1 + exp[(Vh-6)/3])-1. The steady-state inactivation hBa(infinity) varied with holding potential and could be described by the equation hBa(infinity) = [1 + exp(Vh + 10/7)]-1. Recovery from inactivation of IBa was best described by the sum of two exponential time courses with time constants of 300 ms and 1.75 s, respectively. 7. The outward current IK(Ca) developed very slowly (0.5–1 s to half-maximal amplitude) and did not inactivate during a 20-s depolarizing command pulse. Tail current decay of IK(Ca) followed a single exponential time course with voltage-dependent time constants of between 360 and 960 ms. The steady-state activation n infinity of IK(Ca) increased sigmoidally with depolarization as described by the equation n infinity = [1 + exp(Vh-13.5)/-8)]-1. 8. The reversal potentials of IK(Ca) tail currents were close to the expected equilibrium potential for potassium and they varied linearly with log [K]o with a slope of 51 mV. These results suggest a high selectivity of the conductance for K ions.(ABSTRACT TRUNCATED AT 400 WORDS)

Transient and delayed potassium currents in the Retzius cell of the leech, Macrobdella decora

1986 ◽  
Vol 56 (3) ◽  
pp. 812-822 ◽  
Author(s):  
J. Johansen ◽  
A. L. Kleinhaus
Keyword(s):  
Steady State ◽  
Time Constant ◽  
Time Course ◽  
Substantial Part ◽  
Macrobdella Decora ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
K Current ◽  
Retzius Cell ◽  
T Tau

The properties of a quickly inactivating transient K current (IA) and a slowly inactivating delayed K current (IK) were investigated with two-electrode voltage-clamp techniques in the isolated soma of the Retzius cell of the leech, Macrobdella decora. The two currents could be pharmacologically separated according to their different sensitivities to tetraethylammonium ions (TEA) and 4-aminopyridine (4-AP). IA was totally blocked by 3 mM 4-AP but not affected by 25 mM TEA. IK was suppressed almost completely by 25 mM TEA, whereas its peak amplitude only decreased by 10-15% in 3 mM 4-AP. IA was activated at membrane potentials more positive than -35 to -30 mV, whereas the threshold for IK was at more positive potentials of approximately -20 to -15 mV. The activation of IA was rapid with a voltage-dependent time constant [tau m(A)] that varied from 6 to 2 ms for command potentials between -20 and 10 mV (at 22-24 degrees C). The inactivation, which was independent of voltage, was somewhat slower with a time constant (tau A) of approximately 90-110 ms. The time constants for activation [tau m(K)] and the early inactivation phase (tau K) of IK were both voltage dependent. In the range of potential steps from 0 to 30 mV, tau m(K) varied from 12 to 4.5 ms and tau K from 1,500 to 700 ms. The steady-state inactivation of IA varied with holding potential and was complete at potentials more positive than -30 mV. IA was fully available from potentials more negative than -70 mV. IK did not show steady-state inactivation below its threshold of activation. The time course of IA during a maintained depolarization could be reasonably described by the expression IA(t) = IA(infinity) [1-exp(-t/tau m(A))]2 exp(-t/tau A). The time course of activation of IK without allowance for inactivation was approximated by the expression IK(t) = IK(infinity) [1-exp(-t/tau m(K))]2. The reversal potentials and magnitude of both IA and IK were dependent on extra-cellular K concentration, which suggest that a substantial part of the two currents was carried by K ions.

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)

Presynaptic inhibition produced by an identified presynaptic inhibitory neuron. I. Physiological mechanisms

1986 ◽  
Vol 55 (1) ◽  
pp. 113-130 ◽  
Author(s):  
R. Kretz ◽  
E. Shapiro ◽  
E. R. Kandel
Keyword(s):  
Voltage Clamp ◽  
Presynaptic Inhibition ◽  
Inhibitory Neuron ◽  
Outward Current ◽  
Membrane Potentials ◽  
Slow Inward Current ◽  
Synaptic Potential ◽  
Synaptic Current ◽  
Voltage Dependent ◽  
Stimulation Of

We have examined the synaptic conductance mechanisms underlying presynaptic inhibition in Aplysia californica in a circuit in which all the neural elements are identified cells (Fig. 1). L10 makes connections to identified follower cells (RB and left upper quadrant cells, L2-L6). These connections are presynaptically inhibited by stimulating cells of the L32 cluster (4). L32 cells produce a slow inhibitory synaptic potential on L10. This inhibitory synaptic potential is associated with an apparent increased membrane conductance in L10. Both the inhibitory postsynaptic potential (IPSP) and the conductance increase are voltage dependent; the IPSP could not be reversed by hyperpolarizing the membrane potentials to - 120 mV. The hyperpolarization of L10 induced by L32 reduces the transmitter output of L10 and thereby contributes to presynaptic inhibition. However, this hyperpolarization accounts for about 30% of the effect because presynaptic inhibition can still be observed even when the hyperpolarization of L10 by L32 is prevented by voltage clamping. When L10 is voltage clamped, stimulation of L32 produces a slow outward synaptic current associated with an apparent increased conductance. Both the synaptic current and conductance change measured under clamp are voltage dependent, and the outward current could not be reversed. This synaptic current is not mediated by an increase in C1- conductance. It is sensitive to external K+ concentration, especially at hyperpolarized membrane potentials. With L10 under voltage clamp, stimulation of L32 also reduces a slow inward current in L10. This current has time and voltage characteristics similar to those of the Ca2+ current. Presynaptic inhibition is still produced by L32 when L10 is voltage clamped, and transmitter release is elicited by depolarizing voltage-clamp pulses. This component of presynaptic inhibition, which accounts for approximately 70% of the inhibition, appears to be due to a decrease in the Ca2+ current in the presynaptic neuron.

Characterization and functional consequences of delayed rectifier current transient in ventricular repolarization

2000 ◽  
Vol 278 (3) ◽  
pp. H806-H817 ◽  
Author(s):  
Gary A. Gintant
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Inward Rectifier ◽  
Ventricular Repolarization ◽  
Delayed Rectifier ◽  
Voltage Range ◽  
Delayed Rectifier Current ◽  
Recovery From Inactivation ◽  
Voltage Dependent

Although inactivation of the rapidly activating delayed rectifier current ( I Kr) limits outward current on depolarization, the role of I Kr (and recovery from inactivation) during repolarization is uncertain. To characterize I Krduring ventricular repolarization (and compare with the inward rectifier current, I K1), voltage-clamp waveforms simulating the action potential were applied to canine ventricular, atrial, and Purkinje myocytes. In ventricular myocytes, I Kr was minimal at plateau potentials but transiently increased during repolarizing ramps. The I Kr transient was unaffected by repolarization rate and maximal after 150-ms depolarizations (+25 mV). Action potential clamps revealed the I Kr transient terminating the plateau. Although peak I Kr transient density was relatively uniform among myocytes, potentials characterizing the peak transients were widely dispersed. In contrast, peak inward rectifier current ( I K1) density during repolarization was dispersed, whereas potentials characterizing I K1 defined a narrower (more negative) voltage range. In summary, rapidly activating I Kr provides a delayed voltage-dependent (and functionally time-independent) outward transient during ventricular repolarization, consistent with rapid recovery from inactivation. The heterogeneous voltage dependence of I Kr provides a novel means for modulating the contribution of this current during repolarization.

Effects of ACh and adenosine mediated by Kir3.1 and Kir3.4 on ferret ventricular cells

2002 ◽  
Vol 283 (2) ◽  
pp. H615-H630 ◽  
Author(s):  
H. Dobrzynski ◽  
N. C. Janvier ◽  
R. Leach ◽  
J. B. C. Findlay ◽  
M. R. Boyett
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Current Clamp ◽  
Inotropic Effects ◽  
Clamp Technique ◽  
Action Potential Clamp ◽  
Ventricular Cells ◽  
Action Potential Waveform ◽  
Potential Waveform ◽  
Action Potential Shortening

The inotropic effects of ACh and adenosine on ferret ventricular cells were investigated with the action potential-clamp technique. Under current clamp, both agonists resulted in action potential shortening and a decrease in contraction. Under action potential clamp, both agonists failed to decrease contraction substantially. In the absence of agonist, application of the short action potential waveform (recorded previously in the presence of agonist) also resulted in a decrease in contraction. Under action potential clamp, application of ACh resulted in a Ba2+-sensitive outward current with the characteristics of muscarinic K+ current ( I K,ACh); the presence of the muscarinic K+ channel was confirmed by PCR and immunocytochemistry. In the absence of agonist, on application of the short ACh action potential waveform, the decrease in contraction was accompanied by loss of the inward Na+/Ca2+exchange current ( I NaCa). ACh also inhibited the background inward K+ current ( I K,1). It is concluded that ACh activates I K,ACh, inhibits I K,1, and indirectly inhibits I NaCa; this results in action potential shortening, decrease in contraction, and, as a result of the inhibition of I K,1, minimum decrease in excitability.

Modulation of the delayed rectifier, IK, by cadmium in cat ventricular myocytes

1992 ◽  
Vol 262 (1) ◽  
pp. C75-C83 ◽  
Author(s):  
C. H. Follmer ◽  
N. J. Lodge ◽  
C. A. Cullinan ◽  
T. J. Colatsky
Keyword(s):  
Voltage Clamp ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Membrane Potentials ◽  
Delayed Rectifier ◽  
Voltage Range ◽  
Control Value ◽  
Current Voltage ◽  
Voltage Dependent ◽  
Slope Factor

The effects of cadmium on the delayed outward potassium current (IK) were investigated in isolated cat ventricular myocytes using the single suction pipette voltage-clamp technique. IK activation was examined using peak tail currents elicited after 750-ms voltage-clamp steps to selected membrane potentials from a holding potential of -40 mV. In the presence of Cd2+ (0.2 mM), peak tail currents increased from a control value of 85 +/- 12 to 125 +/- 18 pA (n = 4). Activation curves constructed from the average peak tail-current measurements in all experiments showed that Cd2+ shifted the voltage dependence of activation to more positive potentials by 16.4 +/- 2.0 mV and increased the slope factor of the activation curve from 6.1 +/- 0.2 to 6.9 +/- 0.2 mV. In the absence of Cd2+, increases in holding potential from -30 to -70 mV had no effect on the magnitude of the peak tail currents, suggesting that the Cd(2+)-induced increase was not the result of a voltage-dependent increase in the number of available K+ channels at the holding potential. Slow voltage ramps from -70 to +70 mV revealed that Cd2+ increased the outward current at membrane potentials positive to +20 mV and shifted the voltage range in which IK inwardly rectified to more positive potentials. The fully activated current-voltage relationship was also shifted to more positive potentials by Cd2+. Cd2+ did not alter channel selectivity for K+.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sevoflurane on inward rectifier K+ current in guinea pig ventricular cardiomyocytes

1997 ◽  
Vol 273 (1) ◽  
pp. H324-H332 ◽  
Author(s):  
A. Stadnicka ◽  
Z. J. Bosnjak ◽  
J. P. Kampine ◽  
W. M. Kwok
Keyword(s):  
Steady State ◽  
Guinea Pig ◽  
Outward Current ◽  
Inward Rectifier ◽  
Equilibrium Potential ◽  
Ventricular Cardiomyocytes ◽  
Steady State Current ◽  
Voltage Dependent ◽  
Current Activation ◽  
Extracellular Side

The effects of sevoflurane on the inward rectifier potassium current (IKIR) were examined in guinea pig ventricular cardiomyocytes using the whole cell patch-clamp methodology. Sevoflurane had a unique dual effect on the steady-state current amplitude, producing a reversible, concentration- and voltage-dependent block of the inward current at potentials negative to the potassium equilibrium potential (EK) but enhancing the outward current positive to EK. Accordingly, the steady-state conductance negative to EK was reduced by sevoflurane, but conductance positive to EK was increased. The chord conductance-voltage relationship showed depolarizing shifts at 0.7, 1.3, and 1.6 mM sevoflurane. When the myocytes were dialyzed with 10 mM Mg2+, but not with 1.0 mM Mg2+, sevoflurane further slowed current activation kinetics. With 10 mM intracellular Mg2+, the outward current enhancement by sevoflurane and the associated shifts in half-activation potential were abolished. Polyamines abolished all effects of sevoflurane on IKIR. With the use of the Woodhull model for voltage-dependent block, we determined the sevoflurane interaction site with the inward rectifier potassium channel to be at an electrical distance of 0.2 from the extracellular side.

Effect of Temperature on Electrical Resonance in Leopard Frog Saccular Hair Cells

1998 ◽  
Vol 79 (1) ◽  
pp. 312-321 ◽  
Author(s):  
M. S. Smotherman ◽  
P. M. Narins
Keyword(s):  
Steady State ◽  
Resonant Frequency ◽  
Hair Cells ◽  
Outward Current ◽  
Leopard Frog ◽  
Effect Of Temperature ◽  
Channel Kinetics ◽  
Resonant Frequencies ◽  
Voltage Dependent ◽  
Electrical Resonance

Smotherman, M. S. and P. M. Narins. Effect of temperature on electrical resonance in leopard frog saccular hair cells. J. Neurophysiol. 79: 312–321, 1998. Leopard frog saccular hair cells exhibit an electrical resonance in response to a depolarizing stimulus that has been proposed to contribute to the tuning properties of the frog sacculus by acting as an electrical band-pass filter. With the whole cell patch-clamp technique, we have investigated the effect of temperature on electrical resonances in isolated saccular hair cells, and we have described the effects of temperature on the currents and channel kinetics underlying electrical resonance. A hair cell's onset resonant frequency in response to a constant depolarizing current pulse increases linearly with temperature at a rate of 11 Hz/1°C, exhibiting a mean Q 10 of 1.7 between 15 and 35°C. However, offset resonant frequencies continue to double every 10°C, exhibiting a mean Q 10 of 2.1. If steady-state voltage during the stimulus is held constant, all oscillatory frequencies increase with a mean Q 10 of 2.1. The average level of steady-state depolarization during a +150-pA depolarizing current pulse decreases with increasing temperature (−6 mV from 15 to 25°C). This temperature-dependent reduction of the steady-state membrane potential causes a shift in the voltage-dependent channel kinetics to slower rates, thus reducing the apparent Q 10 for onset resonant frequencies. The peak outward tail current and net steady-state outward current, which is the sum of a voltage-dependent inward calcium current ( I Ca) and an outward calcium-dependent potassium current ( I K(Ca)), increase with temperature, exhibiting a mean Q 10 of 1.7 between 15 and 25°C. The activation rate ( T 1/2) of the outward current exhibits a mean Q 10 of 2.3 between 15 and 25°C, while the deactivation rate (τrel) exhibits a mean Q 10 of 2.9 over the same temperature range. These results support previous models of the molecular determination of resonant frequency, which have proposed that a combination of I K(Ca) channel kinetics and the overall magnitude of the outward current are primarily responsible for determining the resonant frequency of an isolated hair cell. The robust temperature sensitivity of the hair cell receptor potential contrasts sharply with the temperature-insensitive tuning properties of in vivo saccular nerve fiber recordings. Possible explanations for this discrepancy are discussed.

Sign in / Sign up

Export Citation Format

Share Document