The Effects of External Potassium and Long Duration Voltage Conditioning on the Amplitude of Sodium Currents in the Giant Axon of the Squid, Loligo pealei (original) (raw)
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The Journal of General Physiology, 1969
Isolated giant axons were voltage-clamped in seawater solutions having constant sodium concentrations of 230 mM and variable potassium concentrations of from zero to 210 mM. The inactivation of the initial transient membrane current normally carried by Na+ was studied by measuring the Hodgkin-Huxley h parameter as a function of time. It was found that h reaches a steady-state value within 30 msec in all solutions. The values of h∞, τh, αh,and ßh as functions of membrane potential were determined for various [Ko]. The steady-state values of the h parameter were found to be inversely related, while the time constant, τh, was directly related to external K+ concentration. While the absolute magnitude as well as the slopes of the h∞ vs. membrane potential curves were altered by varying external K+, only the magnitude and not the shape of the corresponding τh curves was altered. Values of the two rate constants, αh and ßh, were calculated from h∞ and τh values. αh is inversely related to...
Evidence for a sodium-dependent potassium conductance in frog myelinated axon
Neuroscience, 1995
After blockade of the voltage-dependent potassium conductances by intracellular application of 4-aminopyridine and tetraethylammonium in frog myelinated axons, a set of brief (0.1 ms) intracellular depolarizing pulses or a long (200 ms) depolarizing pulse evoked a train of action potentials. Under both experimental conditions a hyperpolarizing afterpotential appeared (duration 367 ms ± 34, mean ± S.E., n = 15). The purpose of this study was to investigate the properties of this hyperpolarizing afterpotential. It was found that the hyperpolarizing afterpotential increases in amplitude with: (1) the number of sodium-dependent action potentials; (2) action potential broadening (following potassium channels blockade); and (3) the level of depolarization during a current step. Application of tetrodotoxin prevented the activation of the hyperpolarizing afterpotential by any of the above stimuli. The hyperpolarizing afterpotential was unaffected by: (1) 8-acetyl-strophanthidin, an agent that poisons the electrogenic pumping in the axon; (2) blocking calcium influx with extracellular 10mM magnesium or 2mM manganese; and (3) buffering of the intracellular calcium, using EGTA in the recording microelectrode. Extracellular application of tetraethylammonium, but not 4-aminopyridine, reduced the hyperpolarizing afterpotential. The hyperpolarizing afterpotential reversed at >>-92 mV. Increasing the external potassium concentration from 2 to 10mM shifted the reversal potential +14.5mV, indicating that the hyperpolarizing afterpotential is a potassium mediated conductance. Reducing the extracellular sodium concentration or replacing the external sodium with lithium ions substantially reduced and/or abolished the hyperpolarizing afterpotential. These results are consistent with the presence of a sodium-activated potassium conductance in amphibian myelinated axons and that activation of the conductance is responsible for the hyperpolarizing afterpotential recorded after blocking voltage-dependent potassium conductances with 4-aminopyridine and tetrathylammonium.
The Journal of Physiology, 1988
1. The effects of some neutral clinical and experimental general anaesthetics on the resting potential of normal squid axons and squid axons exposed to tetrodotoxin and 3,4-diaminopyridine have been studied. 2. Depolarizations of 1-4 mV were produced by all the anaesthetics at 'clinical' concentrations in the normal axon. Larger depolarizations (5-11 mV) were produced by the same anaesthetic concentrations in axons exposed to tetrodotoxin and 3,4diaminopyridine. 3. The conductance of axons exposed to tetrodotoxin and either tetraethylammonium or 3,4-diaminopyridine in zero Na+, 430 mM-K+ artificial sea water was examined by voltage clamp and AC bridge techniques. 4. The evidence that this conductance is due predominantly to K+ is discussed. 5. Pre-pulse protocols under voltage clamp have been used to show that part of this conductance arises from the incompletely blocked delayed rectifier. 6. Substantial reductions in this conductance are produced by anaesthetics at clinical' concentrations. 7. It is concluded that there is a component of the K+ conductance of the resting squid axon other than the Hodgkin-Huxley delayed rectifier which is extremely sensitive to anaesthetics and which to an appreciable extent determines the resting potential.
A quantitative description of the sodium current in the rat sympathetic neurone
The Journal of Physiology, 1986
The somata of rat sympathetic neurones were voltage-clamped in vitro at 27 0C using separate intracellular voltage and current micro-electrodes. 2. Na currents were isolated from other current contributions by using: Cd to block the Ca current (ICa) and the related Ca-dependent K current ('K(ca))' and external tetraethylammonium to suppress the delayed rectifier current (IK(v)). The holding potential was maintained at-50 mV to inactivate the fast transient K current (IA) when the IA contamination was unacceptable. 3. Step depolarizations beyond-30 mV activated a fast, transient inward current carried by Na ions; it was suppressed by tetrodotoxin and was absent in Na-free solution. Once activated, INa declined exponentially to zero with a voltage-dependent time constant. The underlying conductance, gNap showed a sigmoidal activation between-30 and + 10 mV, with half-activation at-211 mV and a maximal value (9Na) of 4-44 1sS per neurone. 4. The steady-state inactivation level, h ,, varied with membrane potential, ranging from complete inactivation at-30 mV to minimal inactivation at about-90 mV with a midpoint at-56-2 mV. Double-pulse experiments showed that development and removal of inactivation followed a single-exponential time course; rh was markedly voltage-dependent and ranged from 46 ms at-50 mV to 2-5 ms at-100 mV. 5. Besides the fast inactivation, the Na conductance showed a slow component of inactivation. The steady-state value, s., was maximal at-80 mV and minimal at-40 mV. The removal of slow inactivation is a two-time-constant process, the first with a time constant in the order of hundreds of milliseconds and the second with a time constant of seconds. Slow inactivation onset appeared to be a faster process than its removal. When slow inactivation was fully removed the peak INa increased by a factor of 1-8. 6. INa was well described by assuming it to be proportional to m3h. 7. The temperature dependence of peak INa' rm and Th was studied in the temperature range 17-27 TC and found similar to that reported for other preparations. The Q10 of these parameters allowed the reconstruction of the INa kinetic properties at 37 0C.
The Journal of Membrane Biology, 1975
Inward sodium currents were measured from voltage-clamped giant axons externally perfused with artificial seawater (ASW) solutions containing various concentrations of sodium and potassium ions. The data was analyzed under the assumption that under a constant membrane potential sodium conductance is determined by a specific ion-channel site (SIS) reaction. The sodium current density values were expressed in terms of SIS-reaction rates which were compared, by means of minimization techniques, with those computed for various saturation reaction mechanisms. The following conclusions were drawn:
An analysis of the long-lasting after-hyperpolarization of guinea-pig vagal motoneurones
The Journal of physiology, 1992
1. The long-lasting after-hyperpolarization which characterizes the neurones of the dorsal motor nucleus of the vagus in the guinea-pig was studied in vitro. 2. Following a train of action potentials, vagal motoneurones develop a long-lasting after-hyperpolarization. Two different shapes of long-lasting after-hyperpolarization were encountered: an after-hyperpolarization which slowly (0.6-1.2 s) and monotonically developed to peak value; and a second type of long-lasting after-hyperpolarization where the onset of the slow component appears to be masked by an early, relatively fast component. Both shapes of long-lasting after-hyperpolarization depend on Ca2+ influx and increase as a function of the number of action potentials in the train. 3. A novel procedure was used to analyse the ionic processes which underlie the long-lasting after-hyperpolarization. The neuronal responses to a series of long (7 s) hyperpolarizing current pulses during the long-lasting after-hyperpolarization we...
The ionic mechanism of the slow outward current in Aplysia neurons
Journal of neurophysiology, 1985
A slow outward current associated with spike frequency adaptation has been studied in the giant Aplysia neurons R2 and LP1. The current was observed during 60-s voltage clamp commands to potentials just below spike threshold. The slow outward current shows a marked voltage dependence at membrane potential less negative than -40 mV. The slow outward current is associated with increased membrane conductance. The K+ sensitivity of the slow outward current was studied by varying the extracellular K+ concentration and also by measuring potassium efflux with a K+-sensitive electrode. Both procedures indicated that the slow outward current was K+ dependent. Tail currents following the activation of the slow outward current were examined. They were shown to have a similar potassium sensitivity as the slow outward current and had a reversal potential near the potassium equilibrium potential for these cells. The sensitivity of the slow outward current to known blockers of K+ currents, tetraet...