Oscillation of Membrane Currents During the Action Potential in Chara corallina: Modification and Significance for Repolarisation of the Membrane Potential and Salt Sensitivity

1996 ◽  
Vol 23 (3) ◽  
pp. 361
Author(s):  
J.I Kourie
Keyword(s):  
Time Course ◽  
Outward Current ◽  
Chara Corallina ◽  
Membrane Currents ◽  
Inactivation Kinetics ◽  
Transient Outward Current ◽  
Voltage Dependent ◽  
Current Activation ◽  
K Current ◽  
Kinetics Of

Depolarising voltage-clamp steps in C. corallina induced membrane currents which differ from those of C. inflata in two aspects: (1) The absence of a 'hump', i.e. a transient outward current,Io(max) which is present in C. inflata, and (2) the presence in C, corallina of a voltage-dependent current oscillation, i.e. a succession of decaying peaks. The peaks of the oscillating transient inward current, Ii(max), were voltage dependent and sensitive to block with 9-anthracenecarboxylic acid (9-AC). The oscillating current is carried by C1- and its time course is determined by the activation and inactivation kinetics of C1- channels. Extracellular NaCl delayed current activation, induced a voltage-dependent increase in Ii(max) and a decrease in the steady-state outward K+ current, Is. NaCl increased the occurrence of oscillation and enhanced the amplitude of the oscillating current. Extracellular sorbitol induced an overall reduction in Ii(max) and had virtually no effect on Is. I suggest that the enhancement of the oscillating transient inward CI- current, Ii(max), by NaCl is due to ionic effects of NaCl rather than to its osmotic effects.

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.

Modulation of Kv4 channels, key components of rat ventricular transient outward K+ current, by PKC

1997 ◽  
Vol 273 (4) ◽  
pp. H1775-H1786 ◽  
Author(s):  
Tomoe Y. Nakamura ◽  
William A. Coetzee ◽  
Eleazar Vega-Saenz De Miera ◽  
Michael Artman ◽  
Bernardo Rudy
Keyword(s):  
Outward Current ◽  
Current Evidence ◽  
Inactivation Kinetics ◽  
Transient Outward Current ◽  
Recovery From Inactivation ◽  
Kv4 Channels ◽  
K Current ◽  
Molecular Components ◽  
Kinetics Of ◽  
Pkc Activation

Current evidence suggests that members of the Kv4 subfamily may encode native cardiac transient outward current ( I to). Antisense hybrid-arrest with oligonucleotides targeted to Kv4 mRNAs specifically inhibited rat ventricular I to, supporting this hypothesis. To determine whether protein kinase C (PKC) affects I to by an action on these molecular components, we compared the effects of PKC activation on Kv4.2 and Kv4.3 currents expressed in Xenopus oocytes and rat ventricular I to. Phorbol 12-myristate 13-acetate (PMA) suppressed both Kv4.2 and Kv4.3 currents as well as native I to, but not after preincubation with PKC inhibitors (e.g., chelerythrine). An inactive stereoisomer of PMA had no effect. Phenylephrine or carbachol inhibited Kv4 currents only when coexpressed, respectively, with α1C-adrenergic or M1 muscarinic receptors (this inhibition was also prevented by chelerythrine). The voltage dependence and inactivation kinetics of Kv4.2 were unchanged by PKC, but small effects on the rates of inactivation and recovery from inactivation of native I to were observed. Thus Kv4.2 and Kv4.3 proteins are important subunits of native rat ventricular I to, and PKC appears to reduce this current by affecting the molecular components of the channels mediating I to.

Activators of protein kinase C mimic serotonin-induced modulation of a voltage-dependent potassium current in pleural sensory neurons of Aplysia

1994 ◽  
Vol 72 (3) ◽  
pp. 1240-1249 ◽  
Author(s):  
S. Sugita ◽  
D. A. Baxter ◽  
J. H. Byrne
Keyword(s):  
Protein Kinase ◽  
Voltage Clamp ◽  
Sensory Neurons ◽  
Phorbol Esters ◽  
Outward Current ◽  
Membrane Currents ◽  
Kinase C ◽  
Voltage Dependent ◽  
K Current ◽  
Kinetics Of

1. In the pleural mechanoafferent sensory neurons of Aplysia, serotonin (5-HT)-induced spike broadening consists of at least two components: a cAMP and protein kinase A (PKA)-dependent, rapidly developing component and a protein kinase C (PKC)-dependent, slowly developing component. Voltage-clamp experiments were conducted to identify currents that are modulated by PKC and thus may contribute to the slowly developing component of 5-HT-induced spike broadening. 2. We compared the effects of phorbol esters, activators of PKC, on membrane currents with those of 5-HT. Bath application of 5-HT had complex modulatory effects on currents elicited by voltage-clamp pulses to potentials > 0 mV. The kinetics of both activation and inactivation of the membrane currents were slowed by 5-HT. This led to a decrease in an outward current at the beginning of the voltage-clamp pulse and an increase at the end of the pulse. Previous work has shown that these effects represent, in part, the modulation of a large, voltage-dependent K+ current (IK,V) by 5-HT. 3. Active phorbol esters mimicked some of the actions of 5-HT on membrane currents in that they slowed activation and inactivation kinetics of current responses to voltage-clamp pulses more positive than 0 mV. This led to a decrease in an outward current at the beginning of the pulse and an increase at the end of the pulse. Because inactive phorbols did not mimic the actions of 5-HT, the effects of active phorbol esters appeared to be PKC specific. In addition, preexposure of the sensory neurons to active phorbol esters appeared to occlude the modulatory actions of 5-HT on IK,V. Thus it is likely that modulation of IK,V by 5-HT is mediated, at lease in part, by PKC. 4. To further characterize which currents were modulated by PKC, low concentrations of tetraethylammonium (TEA, 2 mM) were used to block Ca(2+)-activated K+ current (IK,Ca). Low TEA partially blocked the phorbol ester-induced increase of the outward current at the end of voltage-clamp pulses. These results agreed with previous reports that activation of PKC enhanced a fast component of IK,Ca in these sensory neurons. Such an enhancement would lead to an increase in outward current that should be blocked by low TEA. Low TEA, however, did not affect phorbol ester-induced decrease of the outward current at the beginning of pulse, where the predominant current is IK,V, which is less sensitive to TEA.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Dynamics of aminopyridine block of potassium channels in squid axon membrane.

1976 ◽  
Vol 68 (5) ◽  
pp. 519-535 ◽  
Author(s):  
J Z Yeh ◽  
G S Oxford ◽  
C H Wu ◽  
T Narahashi
Keyword(s):  
Time Course ◽  
Membrane Surface ◽  
K Channel ◽  
Dependent Manner ◽  
Squid Axon ◽  
Axon Membrane ◽  
K Channels ◽  
Voltage Dependent ◽  
K Current ◽  
Kinetics Of

Aminopyridines (2-AP, 3-AP, and 4-AP) selectively block K channels of squid axon membranes in a manner dependent upon the membrane potential and the duration and frequency of voltage clamp pulses. They are effective when applied to either the internal or the external membrane surface. The steady-state block of K channels by aminopyridines is more complete for low depolarizations, and is gradually relieved at higher depolarizations. The K current in the presence of aminopyridines rises more slowly than in control, the change being more conspicuous in 3-AP and 4-AP than in 2-AP. Repetitive pulsing relieves the block in a manner dependent upon the duration and interval of pulses. The recovery from block during a given test pulse is enhanced by increasing the duration of a conditioning depolarizing prepulse. The time constant for this recovery is in the range of 10-20 ms in 3-AP and 4-AP, and shorter in 2-AP. Twin pulse experiments with variable pulse intervals have revealed that the time course for re-establishment of block is much slower in 3-AP and 4-AP than in 2-AP. These results suggest that 2-AP interacts with the K channel more rapidly than 3-AP and 4-AP. The more rapid interaction of 2-AP with K channels is reflected in the kinetics of K current which is faster than that observed in 3-AP or 4-AP, and in the pattern of frequency-dependent block which is different from that in 3-AP or 4-AP. The experimental observations are not satisfactorily described by alterations of Hodgkin-Huxley n-type gating units. Rather, the data are consistent with a simple binding scheme incorporating no changes in gating kinetics which conceives of aminopyridine molecules binding to closed K channels and being released from open channels in a voltage-dependent manner.

Kinetics of slow inactivation of persistent sodium current in layer V neurons of mouse neocortical slices

1996 ◽  
Vol 76 (3) ◽  
pp. 2125-2130 ◽  
Author(s):  
I. A. Fleidervish ◽  
M. J. Gutnick
Keyword(s):  
Time Course ◽  
Sodium Current ◽  
Outward Current ◽  
Slow Inactivation ◽  
Voltage Dependent ◽  
Layer V ◽  
Neuronal Functions ◽  
Kinetics Of ◽  
Whole Cell Recordings ◽  
K Currents

1. In whole cell recordings from layer V neurons in slices of mouse somatosensory neocortex, tetrodotoxin (TTX)-sensitive persistent Na+ current (INaP) was studied by blocking K+ currents with intracellular Cs+ and Ca2+ currents with extracellular Cd2+. During slow voltage ramps, INaP began to activate at around -60 mV, and attained a peak at around -25 mV. The peak amplitude of INaP varied widely from cell to cell (range 60-3,160 pA; median 308 pA, n = 77). At potentials more positive than -35 mV, INaP in all cells was superimposed on a large, TTX-resistant outward current. 2. In hybrid clamp experiments, INaP was significantly reduced by a preceding high-frequency train of spikes. 3. INaP underwent pronounced slow inactivation, which was revealed by systematically varying the ramp speed between 233 and 2.33 mV/s, or varying the duration of a depolarizing prepulse between 0.1 and 10 s. 4. Onset of slow inactivation at +20 mV was monoexponential with tau = 2.06 s (n = 17 cells). Recovery from slow inactivation was voltage dependent. It followed a monoexponential time course with tau = 2.31 s (n = 6) at -70 mV and tau = 1.10 s (n = 4) at -90 mV. These values are not significantly different than values previously reported for slow inactivation of fast-inactivating INa. 5. Slow inactivation of neocortical INaP will influence all neuronal functions in which this current plays a role, including spike threshold determination, synaptic integration, and active propagation in dendrites. The kinetics of slow inactivation suggest that it may be a factor not only during extremely intense spiking, but also during periods of "spontaneous" activity.

Layer I neurons of the rat neocortex. II. Voltage-dependent outward currents

1996 ◽  
Vol 76 (2) ◽  
pp. 668-682 ◽  
Author(s):  
F. M. Zhou ◽  
J. J. Hablitz
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Outward Current ◽  
Pyramidal Cells ◽  
Delayed Rectifier ◽  
Transient Outward Current ◽  
Pharmacological Properties ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
Layer I

1. Whole cell patch-clamp techniques, combined with direct visualization of neurons, were used to study voltage-dependent potassium currents in layer 1 neurons and layer II/III pyramidal cells. 2. In the presence of tetrodotoxin, step depolarizations evoked an outward current. This current had a complex waveform and appeared to be a composite of early and late components. The early peak of the composite K+ outward current was larger in layer I neurons. 3. In both layer I and pyramidal cells, the composite outward K+ current could be separated into two components based on kinetic and pharmacological properties. The early component was termed I(A) because it was a transient outward current activating rapidly and then decaying. I(A) was more sensitive to blocking by 4-aminopyridine (4-AP) than tetraethylammonium (TEA). The second component, termed the delayed rectifier or I(DR), activated relatively slowly and did not decay significantly during a 200-ms test pulse. I(DR) was insensitive to blocking by 4-AP at concentrations up to 4 mM and blocked by > 60% by 40-60 mM TEA. 4. I(A) kinetics were examined in the presence of 40-60 mM TEA. Under these conditions, I(A) began to activate between -40 and -30 mV. Half-maximal activation occurred around 0 mV. In both layer I and pyramidal cells, the half-inactivation potential (Vh-inact) was around or more positive than -50 mV. At -60 mV, > 70% of I(A) conductance was available. I(A) decayed along a single exponential time course with a time constant of approximately 15 ms. This decay showed little voltage dependence. 5. In both layer I and pyramidal cells, I(DR) was studied in the presence of 4 mM 4-AP to block I(A) and in saline containing 0.2 mM Ca2+ and 3.6 mM Mg2+ to reduce contributions from Ca2+-dependent K+ currents. Under these conditions, I(DR) began to activate at -35 to -25 mV with Vh-act of 3.6 +/- 4.5 mV (mean +/- SD). The 10-90% rise time of I(DR) was 15 ms at 30 mV. At 2.2 ms after the onset of the command potential to +30 mV, I(DR) could reach a significant amplitude (approximately 1.5 nA in layer I neurons and 2.2 nA in pyramidal cells depending on the cell size). When long test pulses (> or = 1,000 ms) were used, a decay time constant approximately 800 ms at +40 mV was observed. In both layer I and pyramidal cells, steady state inactivation of I(DR) was minimal. 6. These results indicate that I(A) and I(DR) are the two major hyperpolarizing currents in layer I and pyramidal cells. The kinetics and pharmacological properties of I(A) and I(DR) were not significantly different in fast-spiking layer I neurons and regular-spiking layer II/III pyramidal cells. The relatively positive activation threshold (more than or equal to -40 mV) of both I(A) and I(DR) suggest that they do not play a role in neuronal behavior below action potential (AP) threshold and that their properties are more suitable to repolarize AP. The greater density of I(A) in layer I neurons appears responsible for fast spike generation.

Kinetic properties of a transient outward current in rat neocortical neurons

1992 ◽  
Vol 68 (4) ◽  
pp. 1133-1142 ◽  
Author(s):  
M. Andreasen ◽  
J. J. Hablitz
Keyword(s):  
Time Course ◽  
Outward Current ◽  
Transient Outward Current ◽  
Late Component ◽  
Exponential Time ◽  
Neocortical Neurons ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
Slope Factor ◽  
Single Exponential

1. Whole-cell patch-clamp techniques were used to record outward currents in embryonic rat neocortical neurons maintained in culture. In the presence of tetrodotoxin and cadmium, depolarization evoked an outward current with a complex waveform. This outward current consisted of an initial fast transient component and a late, slowly inactivating component. 2. The two outward current components could be separated pharmacologically with the use of tetraethylammonium (TEA) and 4-aminopyridine (4-AP). TEA (20 mM) applied extracellularly completely blocked the late component, unmasking a fast transient outward current (TOC). 4-AP (5 mM) applied extracellularly blocked the early component while reducing the late component by 27.8 +/- 9.7% (mean +/- SE). 3. The TOC activated after a short delay and rose rapidly to a peak. The time to peak was voltage dependent and decreased with depolarization. In the presence of 200 microM extracellular cadmium, activation threshold was around -25 mV, and current amplitude increased with depolarization. The voltage-conductance relationship was well fitted by the use of the Boltzmann equation with a Vm of +19 mV for half activation and a slope factor of +6 mV. 4. On sustained depolarization the TOC rapidly inactivated and decayed to baseline within 500-600 ms. The decay phase followed a single exponential time course with a time constant of 55-65 ms. The decay time was most rapid at potentials from +5 to +20 mV and increased slightly with further depolarization. 5. Steady-state inactivation of the TOC, in the presence of cadmium, was complete near -10 mV and was totally relieved at potentials more negative than -75 mV. With the use of the Boltzmann equation, a Vm of -34 mV for half inactivation and a slope factor of -8.6 mV were found. 6. Recovery of the TOC from steady-state inactivation followed a single exponential time course and was voltage dependent. When the membrane potential was held at -84 mV during the conditioning pulse, the time constant of recovery was 17 ms, increasing to 45.2 and 58.1 ms at holding potentials of -64 and -44 mV, respectively. Holding at potentials more negative than -84 mV produced no further change in the recovery time course. 7. The presence of 200 microM external cadmium altered the TOC activation and inactivation curves. Removal of cadmium produced a -16-mV shift in the Vm for half activation and a -25-mV shift in the inactivation curve. This sensitivity to cadmium is higher than that reported in other systems.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Excitation-contraction coupling in cardiac Purkinje fibers. Effects of caffeine on the intracellular [Ca2+] transient, membrane currents, and contraction.

1984 ◽  
Vol 83 (3) ◽  
pp. 417-433 ◽  
Author(s):  
P Hess ◽  
W G Wier
Keyword(s):  
Steady State ◽  
Time Course ◽  
Positive Inotropic Effect ◽  
Outward Current ◽  
Membrane Currents ◽  
Slow Inward Current ◽  
Transient Outward Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
L1 And L2

The effects of caffeine on tension, membrane potential, membrane currents, and intracellular [Ca2+], measured as the light emitted by the Ca2+-activated photoprotein aequorin, were studied in canine cardiac Purkinje fibers. An initial, transient, positive inotropic effect of caffeine was accompanied by a transient increase in the second component of the aequorin signal (L2) but not the first (L1). In the steady state, 4 or 10 mM caffeine always decreased twitch tension and greatly reduced both L1 and L2. At a concentration of 2 mM, caffeine usually reduced but occasionally increased the steady state twitch tension. However, 2 mM caffeine always reduced both L1 and L2. Caffeine eliminated the diastolic oscillations of intracellular [Ca2+] induced by high extracellular [Ca2+]. In voltage-clamp experiments, 10 mM caffeine reduced the transient outward current and the peak tension elicited by step depolarization from a holding potential of -45 mV. In the presence of 20 mM Cs+, 10 mM caffeine reduced slow inward current. However, the time course of this reduction was far slower than that in tension and light observed in separate experiments. The simplest explanation of the results is that caffeine inhibits the sequestration of Ca2+ by the sarcoplasmic reticulum. The results also suggest that in Purkinje fibers caffeine increases the sensitivity of the myofilaments to Ca2+.

scholarly journals Rapid recovery from K current inactivation on membrane hyperpolarization in molluscan neurons.

1984 ◽  
Vol 84 (6) ◽  
pp. 861-875 ◽  
Author(s):  
P Ruben ◽  
S Thompson
Keyword(s):  
Time Course ◽  
Outward Current ◽  
Rapid Recovery ◽  
Resting Potential ◽  
Molluscan Neurons ◽  
Membrane Hyperpolarization ◽  
Time Constants ◽  
Recovery From Inactivation ◽  
Voltage Dependent ◽  
K Current

Recovery from K current inactivation was studied in molluscan neurons using two-microelectrode and internal perfusion voltage clamps. Experiments were designed to study the voltage-dependent delayed outward current (IK) without contamination from other K currents. The amount of recovery from inactivation and the rate of recovery increase dramatically when the membrane potential is made more negative. The time course of recovery at the resting potential, -40 mV, is well fit by a single exponential with a time constant of 24.5 s (n = 7). At more negative voltages, the time course is best fit by the sum of two exponentials with time constants at -90 mV of 1.7 and 9.8 s (n = 7). In unclamped cells, a short hyperpolarization can cause rapid recovery from inactivation that results in a shortening of the action potential duration. We conclude that there are two inactivated states of the channel and that the time constants for recovery from both states are voltage dependent. The results are discussed in terms of the multistate model for K channel gating that was developed by R. N. Aldrich (1981, Biophys. J., 36:519-532).

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)

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