scholarly journals Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

1988 ◽  
Vol 91 (4) ◽  
pp. 593-615 ◽  
Author(s):  
R D Harvey ◽  
R E Ten Eick
Keyword(s):  
Steady State ◽  
Time Course ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Inward Current ◽  
Steady State Current ◽  
Voltage Dependent ◽  
K Current ◽  
K Concentration

Whole-cell membrane currents were measured in isolated cat ventricular myocytes using a suction-electrode voltage-clamp technique. An inward-rectifying current was identified that exhibited a time-dependent activation. The peak current appeared to have a linear voltage dependence at membrane potentials negative to the reversal potential. Inward current was sensitive to K channel blockers. In addition, varying the extracellular K+ concentration caused changes in the reversal potential and slope conductance expected for a K+ current. The voltage dependence of the chord conductance exhibited a sigmoidal relationship, increasing at more negative membrane potentials. Increasing the extracellular K+ concentration increased the maximal level of conductance and caused a shift in the relationship that was directly proportional to the change in reversal potential. Activation of the current followed a monoexponential time course, and the time constant of activation exhibited a monoexponential dependence on membrane potential. Increasing the extracellular K+ concentration caused a shift of this relationship that was directly proportional to the change in reversal potential. Inactivation of inward current became evident at more negative potentials, resulting in a negative slope region of the steady state current-voltage relationship between -140 and -180 mV. Steady state inactivation exhibited a sigmoidal voltage dependence, and recovery from inactivation followed a monoexponential time course. Removing extracellular Na+ caused a decrease in the slope of the steady state current-voltage relationship at potentials negative to -140 mV, as well as a decrease of the conductance of inward current. It was concluded that this current was IK1, the inward-rectifying K+ current found in multicellular cardiac preparations. The K+ and voltage sensitivity of IK1 activation resembled that found for the inward-rectifying K+ currents in frog skeletal muscle and various egg cell preparations. Inactivation of IK1 in isolated ventricular myocytes was viewed as being the result of two processes: the first involves a voltage-dependent change in conductance; the second involves depletion of K+ from extracellular spaces. The voltage-dependent component of inactivation was associated with the presence of extracellular Na+.

scholarly journals Voltage-dependent block of cardiac inward-rectifying potassium current by monovalent cations.

1989 ◽  
Vol 94 (2) ◽  
pp. 349-361 ◽  
Author(s):  
R D Harvey ◽  
R E Ten Eick
Keyword(s):  
Ventricular Myocytes ◽  
Negative Slope ◽  
Voltage Sensitivity ◽  
Dependent Manner ◽  
Inward Current ◽  
Current Voltage ◽  
Steady State Current ◽  
Voltage Dependent ◽  
Current Block ◽  
K Current

The inward-rectifying K+ current (IK1) in cat ventricular myocytes, like inward-rectifying K+ currents in many other preparations, exhibited a negative slope conductance region at hyperpolarized membrane potentials that was time-dependent. This was evident as an inactivation of inward current elicited by hyperpolarizing voltage-clamp pulses resulting in a negative slope region of the steady-state current-voltage relationship at potentials negative to -140 mV. Removing extracellular Na+ prevented the development of the negative slope in this voltage region, suggesting that Na+ can block IK1 channels in a time- and voltage-dependent manner. The time and voltage dependence of Cs+-induced block of IK1 was also examined. Cs+ blocked inward current in a manner similar to that of Na+, but the former was much more potent. The fraction of current blocked by Cs+ in the presence of Na+ was reduced in a time- and voltage-dependent manner, which suggested that these blocking ions compete for a common or at least similar site of action. In the absence of Na+, inactivation of IK1 could also be induced by both Cs+ and Li+. However, Li+ was less potent than Na+ in this respect. Calculation of the voltage sensitivity of current block by each of these ions suggests that the mechanism of block by each is similar.

5-HT modulation of hyperpolarization-activated inward current and calcium-dependent outward current in a crustacean motor neuron

1992 ◽  
Vol 68 (2) ◽  
pp. 496-508 ◽  
Author(s):  
O. Kiehn ◽  
R. M. Harris-Warrick
Keyword(s):  
Motor Neuron ◽  
Time Course ◽  
Reversal Potential ◽  
Outward Current ◽  
Resting Membrane Potential ◽  
Inward Current ◽  
Calcium Dependent ◽  
Voltage Dependent ◽  
K Concentration ◽  
Conductance Increase

1. Serotonergic modulation of a hyperpolarization-activated inward current, Ih, and a calcium-dependent outward current, Io(Ca), was examined in the dorsal gastric (DG) motor neuron, with the use of intracellular recording techniques in an isolated preparation of the crab stomatogastric ganglion (STG). 2. Hyperpolarization of the membrane from rest with maintained current pulses resulted in a slow time-dependent relaxation back toward rest and a depolarizing overshoot after termination of the current pulse. In voltage clamp, hyperpolarizing commands negative to approximately -70 mV caused a slowly developing inward current, Ih, which showed no inactivation. Repolarization back to the holding potential of -50 mV revealed a slow inward tail current. 3. The reversal potential for Ih was approximately -35 mV. Raising extracellular K+ concentration ([K+]o) from 11 to 22 mM enhanced, whereas decreasing extracellular Na+ concentration ([Na+]o) reduced the amplitude of Ih. These results indicate that Ih in DG is carried by both K+ and Na+ ions. 4. Bath application of serotonin (5-HT; 10 microM) caused a marked increase in the amplitude of Ih through its active voltage ranges. 5. The time course of activation of Ih was well fitted by a single exponential function and strongly voltage dependent. 5-HT increased the rate of activation of Ih. 5-HT also slowed the rate of deactivation of the Ih tail on repolarization to -50 mV. 6. The activation curve for the conductance (Gh) underlying Ih was obtained by analyzing tail currents. 5-HT shifted the half activation for Gh from approximately -105 mV in control to -95 mV, resulting in an increase in the amplitude of Gh active at rest. 7. Two to 4 mM Cs+ abolished Ih, whereas barium (200 microM to 2 mM) had only weak suppressing effects on Ih. Concomitantly, Cs+ also blocked the 5-HT-induced inward current and conductance increase seen at voltages negative to rest. In current clamp, Cs+ caused DG to hyperpolarize 3-4 mV from rest, suggesting that Ih is partially active at rest and contributes to the resting membrane potential. 8. Depolarizing voltage commands from a holding potential of -50 mV resulted in a total outward current (Io) with an initial transient component and a sustained steady-state component. Application of 5-HT reduced both the transient and sustained components of Io. 9. Io was reduced by 10-20 mM tetraethylammonium (TEA), suggesting that it is primarily a K+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

Characteristics and postnatal development of a hyperpolarization-activated inward current in rat hypoglossal motoneurons in vitro

1994 ◽  
Vol 71 (1) ◽  
pp. 119-128 ◽  
Author(s):  
D. A. Bayliss ◽  
F. Viana ◽  
M. C. Bellingham ◽  
A. J. Berger
Keyword(s):  
Postnatal Development ◽  
Voltage Dependence ◽  
Reversal Potential ◽  
Membrane Potentials ◽  
Time Constants ◽  
Inward Current ◽  
Hypoglossal Motoneurons ◽  
Tail Current ◽  
Cationic Current ◽  
Voltage Dependent

1. Single-electrode voltage clamp recordings in a rat brain stem slice preparation were used to determine the characteristics and postnatal development of a hyperpolarization-activated inward current (Ih) in hypoglossal motoneurons (HMs). 2. In young adult HMs (> P21), a noninactivating, time- and voltage-dependent inward current was evident during hyperpolarizing voltage steps to membrane potentials negative to approximately -65 mV from depolarized holding potentials [Vh = -56.2 +/- 1.0 (SE) mV]. The averaged reversal potential (Erev) of the inward current, estimated using an extrapolation procedure, was -38.8 +/- 2.9 mV (n = 5), suggesting that a mixed cationic current underlies inward rectification in HMs. 3. The voltage dependence of Ih activation was determined from tail current relaxations that followed a family of voltage steps to different membrane potentials. Normalized tail current amplitudes were well-fitted with a single Boltzman function with a half-activation at -79.8 +/- 0.7 mV and slope factor = 5.3 +/- 0.3 (n = 8). 4. Time constants of Ih activation and deactivation were voltage-dependent. Activation proceeded more quickly with larger hyperpolarizing voltage steps; time constants averaged 389, 181, and 134 ms at -69, -82, and -95 mV, respectively (n = 6). Ih deactivated during depolarizing voltage steps from hyperpolarized holding potentials. Deactivation was faster with larger depolarizing steps; time constants averaged 321, 215, and 107 ms at -80, -71, and -62 mV, respectively (n = 4). 5. Ih was sensitive to extracellular cesium but relatively insensitive to extracellular barium. The current amplitude near half-activation (approximately -84 mV) was almost completely blocked (to 11% of control) by Cs+ (3 mM, n = 3) but was reduced to only 85 and 60% in 0.5 (n = 2) and 2 mM Ba2+ (n = 3), respectively. 6. There was a marked increase in the amplitude of Ih during postnatal development of HMs. Measured near half-activation, Ih was approximately 10-fold larger in adult (> or = P21; n = 20) than in neonatal HMs (< or = P8; n = 7). Input conductance (GN) was only threefold higher in the same sample of HMs. There were no apparent differences in the voltage dependence or Erev of Ih between neonatal and older HMs. These results suggest that the increased amplitude of Ih results from an increase in Ih current density.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals A time- and voltage-dependent K+ current in single cardiac cells from bullfrog atrium.

1986 ◽  
Vol 88 (6) ◽  
pp. 777-798 ◽  
Author(s):  
J R Hume ◽  
W Giles ◽  
K Robinson ◽  
E F Shibata ◽  
R D Nathan ◽  
...  
Keyword(s):  
Time Course ◽  
Voltage Dependence ◽  
Outward Current ◽  
Cardiac Cells ◽  
Delayed Rectifier ◽  
Mechanical Dispersion ◽  
Atrial Cells ◽  
Voltage Dependent ◽  
K Current ◽  
Kinetics Of

Individual myocytes were isolated from bullfrog atrium by enzymatic and mechanical dispersion, and a one-microelectrode voltage clamp was used to record the slow outward K+ currents. In normal [K+]o (2.5 mM), the slow outward current tails reverse between -95 and -100 mV. This finding, and the observed 51-mV shift of Erev/10-fold change in [K+]o, strongly suggest that the "delayed rectifier" in bullfrog atrial cells is a K+ current. This current, IK, plays an important role in initiating repolarization, and it is distinct from the quasi-instantaneous, inwardly rectifying background current, IK. In atrial cells, IK does not exhibit inactivation, and very long depolarizing clamp steps (20 s) can be applied without producing extracellular K+ accumulation. The possibility of [K+]o accumulation contributing to these slow outward current changes was assessed by (a) comparing reversal potentials measured after short (2 s) and very long (15 s) activating prepulses, and (b) studying the kinetics of IK at various holding potentials and after systematically altering [K+]o. In the absence of [K+]o accumulation, the steady state activation curve (n infinity) and fully activated current-voltage (I-V) relation can be obtained directly. The threshold of the n infinity curve is near -50 mV, and it approaches a maximum at +20 mV; the half-activation point is approximately -16 mV. The fully activated I-V curve of IK is approximately linear in the range -40 to +30 mV. Semilog plots of the current tails show that each tail is a single-exponential function, which suggests that only one Hodgkin-Huxley conductance underlies this slow outward current. Quantitative analysis of the time course of onset of IK and of the corresponding envelope of tails demonstrate that the activation variable, n, must be raised to the second power to fit the sigmoid onset accurately. The voltage dependence of the kinetics of IK was studied by recording and curve-fitting activating and deactivating (tail) currents. The resulting 1/tau n curve is U-shaped and somewhat asymmetric; IK exhibits strong voltage dependence in the diastolic range of potentials. Changes in the [Ca2+]o in the superfusing Ringer's, and/or addition of La3+ to block the transmembrane Ca2+ current, show that the time course and magnitude of IK are not significantly modulated by transmembrane Ca2+ movements, i.e., by ICa. These experimentally measured voltage- and time-dependent descriptors of IK strongly suggest an important functional role for IK in atrial tissue: it initiates repolarization and can be an important determinant of rate-induced changes in action potential duration.

scholarly journals The calcium-independent transient outward potassium current in isolated ferret right ventricular myocytes. I. Basic characterization and kinetic analysis.

1993 ◽  
Vol 101 (4) ◽  
pp. 571-601 ◽  
Author(s):  
D L Campbell ◽  
R L Rasmusson ◽  
Y Qu ◽  
H C Strauss
Keyword(s):  
Steady State ◽  
Ventricular Myocytes ◽  
Nonlinear Least Squares ◽  
Patch Clamp Technique ◽  
Time Constants ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
K Current ◽  
Necessary And Sufficient

Enzymatically isolated myocytes from ferret right ventricles (12-16 wk, male) were studied using the whole cell patch clamp technique. The macroscopic properties of a transient outward K+ current I(to) were quantified. I(to) is selective for K+, with a PNa/PK of 0.082. Activation of I(to) is a voltage-dependent process, with both activation and inactivation being independent of Na+ or Ca2+ influx. Steady-state inactivation is well described by a single Boltzmann relationship (V1/2 = -13.5 mV; k = 5.6 mV). Substantial inactivation can occur during a subthreshold depolarization without any measurable macroscopic current. Both development of and recovery from inactivation are well described by single exponential processes. Ensemble averages of single I(to) channel currents recorded in cell-attached patches reproduce macroscopic I(to) and indicate that inactivation is complete at depolarized potentials. The overall inactivation/recovery time constant curve has a bell-shaped potential dependence that peaks between -10 and -20 mV, with time constants (22 degrees C) ranging from 23 ms (-90 mV) to 304 ms (-10 mV). Steady-state activation displays a sigmoidal dependence on membrane potential, with a net aggregate half-activation potential of +22.5 mV. Activation kinetics (0 to +70 mV, 22 degrees C) are rapid, with I(to) peaking in approximately 5-15 ms at +50 mV. Experiments conducted at reduced temperatures (12 degrees C) demonstrate that activation occurs with a time delay. A nonlinear least-squares analysis indicates that three closed kinetic states are necessary and sufficient to model activation. Derived time constants of activation (22 degrees C) ranged from 10 ms (+10 mV) to 2 ms (+70 mV). Within the framework of Hodgkin-Huxley formalism, Ito gating can be described using an a3i formulation.

Is there an A-type K+ current in guinea pig ventricular myocytes?

2003 ◽  
Vol 284 (2) ◽  
pp. H598-H604 ◽  
Author(s):  
Ian Findlay
Keyword(s):  
Guinea Pig ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Outward Current ◽  
Type K ◽  
K Current

A unique transient outward K+ current ( I to) has been described to result from the removal of extracellular Ca2+ from ventricular myocytes of the guinea pig (15). This study addressed the question of whether this current represented K+-selective I to or the efflux of K+ via L-type Ca2+ channels. This outward current was inhibited by Cd2+, Ni2+, Co2+, and La3+ as well as by nifedipine. All of these compounds were equally effective inhibitors of the L-type Ca2+ current. The current was not inhibited by 4-aminopyridine. Apparent inhibition of the outward current by extracellular Ca2+ was shown to result from the displacement of the reversal potential of cation flux through L-type Ca2+ channels. The current was found not to be K+ selective but also permeant to Cs+. The voltage dependence of inactivation of the outward current was identical to that of the L-type Ca2+ current. It is concluded that extracellular Ca2+ does not mask an A-type K+current in guinea pig ventricular myocytes.

scholarly journals Na Self Inhibition of Human Epithelial Na Channel

2002 ◽  
Vol 120 (2) ◽  
pp. 133-145 ◽  
Author(s):  
Ahmed Chraïbi ◽  
Jean-Daniel Horisberger
Keyword(s):  
Steady State ◽  
Reversal Potential ◽  
Outward Current ◽  
Inactivation Rate ◽  
Na Channel ◽  
Temperature Dependent ◽  
Open Probability ◽  
Inward Current ◽  
Steady State Current ◽  
Epithelial Na Channel

The regulation of the open probability of the epithelial Na+ channel (ENaC) by the extracellular concentration of Na+, a phenomenon called “Na+ self inhibition,” has been well described in several natural tight epithelia, but its molecular mechanism is not known. We have studied the kinetics of Na+ self inhibition on human ENaC expressed in Xenopus oocytes. Rapid removal of amiloride or rapid increase in the extracellular Na+ concentration from 1 to 100 mM resulted in a peak inward current followed by a decline to a lower quasi-steady-state current. The rate of current decline and the steady-state level were temperature dependent and the current transient could be well explained by a two-state (active-inactive) model with a weakly temperature-dependent (Q10act = 1.5) activation rate and a strongly temperature-dependant (Q10inact = 8.0) inactivation rate. The steep temperature dependence of the inactivation rate resulted in the paradoxical decrease in the steady-state amiloride-sensitive current at high temperature. Na+ self inhibition depended only on the extracellular Na+ concentration but not on the amplitude of the inward current, and it was observed as a decrease of the conductance at the reversal potential for Na+ as well as a reduction of Na+ outward current. Self inhibition could be prevented by exposure to extracellular protease, a treatment known to activate ENaC or by treatment with p-CMB. After protease treatment, the amiloride-sensitive current displayed the expected increase with rising temperature. These results indicate that Na+ self inhibition is an intrinsic property of sodium channels resulting from the expression of the α, β, and γ subunits of human ENaC in Xenopus oocyte. The extracellular Na+-dependent inactivation has a large energy of activation and can be abolished by treatment with extracellular proteases.

scholarly journals The Ventral Photoreceptor Cells of Limulus

1969 ◽  
Vol 54 (3) ◽  
pp. 331-351 ◽  
Author(s):  
Ronald Millecchia ◽  
Alexander Mauro
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Dark Current ◽  
Time Course ◽  
Reversal Potential ◽  
Negative Slope ◽  
Induced Current ◽  
Current Voltage ◽  
Steady State Current ◽  
Current Voltage Relation

In the dark, the ventral photoreceptor of Limulus exhibits time-variant currents under voltage-clamp conditions; that is, if the membrane potential of the cell is clamped to a depolarized value there is an initial large outward current which slowly declines to a steady level. The current-voltage relation of the cell in the dark is nonlinear. The only ion tested which has any effect on the current-voltage relation is potassium; high potassium shifts the reversal potential towards zero and introduces a negative slope-conductance region. When the cell is illuminated under voltage-clamp conditions, an additional current, the light-induced current, flows across the cell membrane. The time course of this current mimics the time course of the light response (receptor potential) in the unclamped cell; namely, an initial transient phase is followed by a steady-state phase. The amplitude of the peak transient current can be as large as 60 times the amplitude of the steady-state current, while in the unclamped cell the amplitude of the peak transient voltage never exceeds 4 times the amplitude of the steady-state voltage. The current-voltage relations of the additional light-induced current obtained for different instants of time are also nonlinear, but differ from the current-voltage relations of the dark current. The ions tested which have the greatest effect on the light-induced current are sodium and calcium; low sodium decreases the current, while low calcium increases the current. The data strongly support the hypothesis that two systems of electric current exist in the membrane. Thus the total ionic current which flows in the membrane is accounted for as the sum of a dark current and a light-induced current.

1S,3R-ACPD Induces a Region of Negative Slope Conductance in the Steady-State Current-Voltage Relationship of Hippocampal Pyramidal Cells

1997 ◽  
Vol 77 (1) ◽  
pp. 221-228 ◽  
Author(s):  
Anita Lüthi ◽  
Beat H. Gähwiler ◽  
Urs Gerber
Keyword(s):  
Steady State ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Resting Potential ◽  
Negative Slope ◽  
Inward Current ◽  
Current Voltage ◽  
Steady State Current ◽  
Current Voltage Relationship ◽  
Voltage Relationship

Lüthi, Anita, Beat H. Gähwiler, and Urs Gerber. 1 S,3 R-ACPD induces a region of negative slope conductance in the steady-state current-voltage relationship of hippocampal pyramidal cells. J. Neurophysiol. 77: 221–228, 1997. Synaptic responses mediated by metabotropic glutamate receptors (mGluRs) display a marked voltage-dependent increase in amplitude when neurons are moderately depolarized beyond membrane potential. We have investigated the basis for this apparent nonlinear behavior by activatingmGluRs with 1 S,3 R-1-aminocyclopentane-1,3-dicarboxylate(1 S,3 R-ACPD; 10 μM) in CA3 pyramidal cells from rat hippocampal slice cultures with the use of the single-electrode voltage-clamp technique. Under control conditions, cells depolarized from resting potential by 10–20 mV responded with delayed outwardly rectifying currents due to activation of voltage- and Ca2+-dependent K+ conductances. In contrast, in the continuous presence of 1 S,3 R-ACPD, small depolarizations (10–20 mV) induced a delayed inward current. The steady-state current-voltage relationship for this response displayed a region of negative slope conductance at potentials between −55 and −40 mV. The reversal potential of the corresponding 1 S,3 R-ACPD-sensitive tail currents (−93.0 ± 2.2 mV, mean ± SE) was close to the potassium reversal potential, consistent with an mGluR-mediated suppression of K+ current. When external K+ concentration was increased to 8 mM, there was a positive shift in reversal potential to −76.9 ± 5.1 mV. The depolarization-induced inward current in the presence of 1 S,3 R-ACPD was blocked by Ba2+ (1 mM). The response was not dependent on changes in intracellular Ca2+ concentration and was insensitive to bath-applied Cs+ (1 mM), ruling out a contribution of Ca2+-dependent currents or the inward rectifier I Q. Furthermore, the effect of 1 S,3 R-ACPD was not mimicked by inhibiting afterhyperpolarizing current and M current with low-Ca2+ saline (0.5 mM Ca2+, 10 mM Mg2+) containing 10 mM tetraethylammonium chloride. A comparison of the responses induced by 1 S,3 R-ACPD and N-methyl-d-aspartate showed that both induce an inward current with small depolarizations from resting potential but with different kinetics and Mg2+ sensitivity. These results indicate that the suppression of K+ currents in response to activation of mGluRs is markedly voltage dependent, increasing at depolarized potentials and decreasing at hyperpolarized potentials. The negative slope conductance at membrane voltages positive to resting potential may underlie the amplification of mGluR-mediated responses when the membrane potential approaches action potential threshold.

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.

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