| The Conditions for Initiating "All-or-Nothing" Repolarization in Cardiac Muscle Biophysical Journal, Volume 3, Issue 4, 1 July 1963, Pages 261-274 D. Noble and A.E. Hall Abstract Solutions have been computed for the point polarization of an infinite cable-like membrane obeying the equations used to reproduce the Purkinje fiber action potential (Noble, 1960, 1962) in order to determine the conditions for initiating all-or-nothing repolarization during the action potential plateau. It was found that all-or-nothing repolarization would not be obtainable during the first half of the action potential in spite of the fact that the membrane current-voltage relations contain regions of negative conductance. At the point at which the all-or-nothing response is first obtained, the computed threshold is large and repolarization almost back to the resting potential would be required in order to initiate the response. The results are discussed in relation to the experimental evidence at present available on repolarization in heart muscle. Abstract | PDF (951 kb) |
| Presynaptic K channels: electrifying regulators of synaptic terminal excitability Trends in Neurosciences, Volume 27, Issue 4, 1 April 2004, Pages 210-217 Paul D. Dodson and Ian D. Forsythe Abstract Potassium channels are crucial regulators of neuronal excitability, setting resting membrane potentials and firing thresholds, repolarizing action potentials and limiting excitability. Although most of our understanding of K channels is based on somatic recordings, there is good evidence that these channels are present in synaptic terminals. In recent years the improved access to presynaptic compartments afforded by direct recording techniques has indicated diverse roles for native K channels, from suppression of aberrant firing to action potential repolarization and activity-dependent modulation of synaptic activity. This article reviews the growing evidence for multiple roles and discrete localization of distinct K channels at presynaptic terminals. Abstract | Full Text | PDF (705 kb) |
| Post-repolarization block of cardiac sodium channels by saxitoxin Biophysical Journal, Volume 65, Issue 2, 1 August 1993, Pages 790-798 J.C. Makielski, J. Satin and Z. Fan Abstract Phasic block of rat cardiac Na+ current by saxitoxin was assessed using pulse trains and two-pulse voltage clamp protocols, and the results were fit to several kinetic models. For brief depolarizations (5 to 50 ms) the depolarization duration did not affect the rate of development or the amplitude of phasic block for pulse trains. The pulse train data were well described by a recurrence relation based upon the guarded receptor model, and it provided rate constants that accurately predicted first-pulse block as well as recovery time constants in response to two-pulse protocols. However, the amplitudes and rates of phasic block development at rapid rates (> 5 Hz) were less than the model predicted. For two pulse protocols with a short (10 ms) conditioning step to -30 mV, block developed only after repolarization to -150 mV and then recovered as the interpulse interval was increased. This suggested that phasic block under these conditions was caused by binding with increased affinity to a state that exists transiently after repolarization to -150 mV. This "post-repolarization block" was fit to a three-state model consisting of a transient state with high affinity for the toxin, the toxin bound state, and the ultimate resting state of the channel. This model accounted for the biphasic post-repolarization block development and recovery observed in two-pulse protocols, and it more accurately described phasic block in pulse trains.(ABSTRACT TRUNCATED AT 250 WORDS) Abstract | PDF (884 kb) |
Copyright © 1980 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 31, Issue 3, 325-331, 1 September 1980
doi:10.1016/S0006-3495(80)85062-4
Research Article
B. Neumcke, W. Schwarz and R. Stämpfli
Asymmetry currents were measured in nodes of myelinated nerve fibers from Rana esculenta at extracellular pH values of 5.2, 7.0, and 8.1 by averaging the currents during and after 1-ms depolarizing and hyperpolarizing voltage pulses. The charge displacement in the nodal membrane was obtained by numerical integration of the asymmetry currents. Lowering the pH from 7.0 to 5.2 significantly slows down the kinetics of the fast charge displacement during depolarization but hardly affects the kinetics after repolarization. The pH reduction increases the maximum charge displacement during depolarization by 46%. No differences between asymmetry currents were found between pH 7.0 and 8.1. It is concluded that protonation by extracellular H+ ions may increase the net charge or the transition range of mobile subunits in the nerve membrane.