Influence of membrane thickness and ion concentration on the properties of the gramicidin A channel Autocorrelation, spectral power density, relaxation and single-channel studies

2. Reduction of the sodium current by depolarizing prepulses had no effect on y, and, in cases where it could be determined, had no significant effect on N. Partial block of the sodium conductance with tetrodotoxin and saxitoxin also did not affect y significantly, but reduced N.3. y was reduced to about 40 % of the control value at -5 mV when the pH of the external solution was reduced to 5 0. The pH dependence of y is consistent with the theories of Woodhull and of Drouin & Neumcke.4. The differing effects of prepulses, toxins and pH are interpreted in view of the different time scales of channel inactivation or block under these conditions. 5. The nearly unchanged y with prepulses and partial toxin block provides further evidence for the absence of interactions among sodium channels.

Section: Discussionmentioning

confidence: 99%

The conductance of sodium channels under conditions of reduced current at the node of Ranvier.

Sigworth¹

1980

“…However, recent observations have shown that permeant ions alter kinetic properties of gramicidin (Kolb & Bamberg, 1977) and nystatin (Ermishkin, Kasumov & Potseluyev, 1977) channels in artificial bilayers, as well as ACh-sensitive (Van Helden et al 1977) and GABA-sensitive (Onodera & Takeuchi, 1979) synaptic channels. It is tempting to relate these effects to a stabilization of the open configuration of the channel by permeant ion binding.…”

Section: Ionic Binding and Kinetics Of Channel Closingmentioning

confidence: 99%

Interaction of permeant ions with channels activated by acetylcholine in Aplysia neurones.

Marchais¹,

Marty²

1979

SUMMARY1. Aplysia neurones with an excitatory response to acetylcholine (ACh) were voltage-clamped, and the ACh-induced currents were studied using noise and relaxation techniques. The mean channel open time, T, and the amplitude of the elementary current, ie1, were determined from these experiments, and the variation of these parameters with the ionic content of the extracellular solution was analysed. The goal of this work was to test whether permeant ions may bind in a voltagedependent manner to channel sites and thereby hinder channel closing, as has been proposed before (Ascher, Marty & Neild, 1978a).2. The relation between T and the membrane potential V has a similar shape in normal sea water and after total replacement of Na ions with Li or Cs. In contrast, the shape of the r(V) relation is modified if Na is replaced by Mg, Sr, or Ba. 5. Experiments were performed in solutions containing Na and sucrose, or Mg and mannitol. In both cases r was smaller than in an isotonic Na or Mg solution.6. None of the above observations can be accounted for on the sole basis of outer surface potential changes.7. A quantitative model of the interaction between permeant ions and AChsensitive channels is proposed. The possible relevance of this model for the interpretation of r( V) curves in other systems is discussed.

“…The different rates of channel opening and closing in Aply8ia may be due to structural differences in the channel proteins or to differences in the lipid environment. In studies on lipids bilayers, the nature of the membrane lipid has been shown to affect channel life time and conductance (Bean, 1973;Kolb & Bamberg, 1977). Moreover, it has been recently reported in Aplyaia neurones (Stephens & Shinitzky, 1977) that the ionic conductance associated with the generation of the action potential is dependent on membrane fluidity determined by the cholesterol level.…”

mentioning

confidence: 99%

Characteristics of sodium and calcium conductance changes produced by membrane depolarization in an Aplysia neurone.

Adams¹,

Gage²

1979

SUMMARY1. The time course and voltage dependence of Na and Ca conductance changes produced by depolarization of the soma of the neurone R15 in the abdominal ganglion of Aplysia juliana were examined at temperatures of 10-14 'C.2. During a maintained depolarization, Na currents turned on then decayed (inactivated). Inactivation was exponential with time constant rh. Activation (after correction for inactivation) was reasonably well described by the expression G' (t) = GNI(oo) (1 -exp [-tIrm])3 over a wide range of potentials. Half-maximal Na conductance occurred at a membrane potential of -8 mV and from -15 to -5 mV, a 5 mV change in membrane potential produced an e-fold change in steady-state Na conductance. 4. Steady-state inactivation of Na conductance (hNa(oo)) was voltage dependent with half-inactivation occurring at a membrance potential of -32 mV. Recovery from Na inactivation followed an exponential time course with a voltage-dependent time constant.5. During a maintained depolarization Ca currents activated then decayed (inactivated) more slowly than Na currents. The decay was exponential with time constant rH. The decay of Ca current was not an artifact produced by an outward current. The amplitude of calcium tail currents, produced by voltage steps back to eK at different times during the decay of Ic., decayed also with a time constant close to TH.6. Ca conductance (after correction for inactivation) could be described approximately by the expression G' (t) = G' (oo) ( 1-exp [-t/TM])P but it was necessary to vary p from 1 to 2 at different potentials. No value of p gave as good a fit to this model as that obtained for Na currents.7. TM and TH were voltage dependent. In the range of potentials from 0 to + 60 mV, TM varied from 9 to 5 msec and TH from 300 to 50 msec (13-5 'C).