Action potentials and membrane currents in the human node of Ranvier

1995 ◽  
Vol 430 (2) ◽  
pp. 283-292 ◽  
Author(s):  
J�rgen R. Schwarz ◽  
Gordon Reid ◽  
Hugh Bostock
Keyword(s):  
Action Potentials ◽  
Node Of Ranvier ◽  
Membrane Currents

Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Patch Clamp Technique ◽  
17Β Estradiol ◽  
Electrophysiological Effects ◽  
Ionic Basis

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.

Effects of pirmenol on action potentials and membrane currents in single atrial myocytes

1998 ◽  
Vol 344 (2-3) ◽  
pp. 287-297 ◽  
Author(s):  
Toshiaki Nakajima ◽  
Kuniaki Iwasawa ◽  
Hisanori Hazama ◽  
Masao Omata
Keyword(s):  
Action Potentials ◽  
Membrane Currents ◽  
Atrial Myocytes

scholarly journals Action Potential Propagation and Synchronisation in Myelinated Axons

2019 ◽  
Author(s):  
Helmut Schmidt ◽  
Thomas R. Knösche
Keyword(s):  
White Matter ◽  
Action Potential ◽  
Myelin Sheath ◽  
Action Potentials ◽  
Structural Parameters ◽  
Node Of Ranvier ◽  
Model Parameters ◽  
Mathematical Framework ◽  
Whole Brain ◽  
Action Potential Propagation

AbstractWith the advent of advanced MRI techniques it has become possible to study axonal white matter non-invasively and in great detail. Measuring the various parameters of the long-range connections of the brain opens up the possibility to build and refine detailed models of large-scale neuronal activity. One particular challenge is to find a mathematical description of action potential propagation that is sufficiently simple, yet still biologically plausible to model signal transmission across entire axonal fibre bundles. We develop a mathematical framework in which we replace the Hodgkin-Huxley dynamics by a spike-diffuse-spike model with passive sub-threshold dynamics and explicit, threshold-activated ion channel currents. This allows us to study in detail the influence of the various model parameters on the action potential velocity and on the entrainment of action potentials between ephaptically coupled fibres without having to recur to numerical simulations. Specifically, we recover known results regarding the influence of axon diameter, node of Ranvier length and internode length on the velocity of action potentials. Additionally, we find that the velocity depends more strongly on the thickness of the myelin sheath than was suggested by previous theoretical studies. We further explain the slowing down and synchronisation of action potentials in ephaptically coupled fibres by their dynamic interaction. In summary, this study presents a solution to incorporate detailed axonal parameters into a whole-brain modelling framework.Author summaryWith more and more data becoming available on white-matter tracts, the need arises to develop modelling frameworks that incorporate these data at the whole-brain level. This requires the development of efficient mathematical schemes to study parameter dependencies that can then be matched with data, in particular the speed of action potentials that cause delays between brain regions. Here, we develop a method that describes the formation of action potentials by threshold activated currents, often referred to as spike-diffuse-spike modelling. A particular focus of our study is the dependence of the speed of action potentials on structural parameters. We find that the diameter of axons and the thickness of the myelin sheath have a strong influence on the speed, whereas the length of myelinated segments and node of Ranvier length have a lesser effect. In addition to examining single axons, we demonstrate that action potentials between nearby axons can synchronise and slow down their propagation speed.

scholarly journals The mechanosensitive ion channel TRAAK is localized to the mammalian node of Ranvier

2019 ◽  
Author(s):  
Stephen G. Brohawn ◽  
Weiwei Wang ◽  
Jürgen R. Schwarz ◽  
Annie Handler ◽  
Ernest B. Campbell ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Polyclonal Antibodies ◽  
Node Of Ranvier ◽  
Nerve Fibers ◽  
Resting Membrane Potential ◽  
Myelinated Nerve ◽  
Myelinated Nerve Fibers ◽  
Behavioral Studies ◽  
Mechanosensitive Ion Channel

ABSTRACTTRAAK is a membrane tension-activated K+ channel that has been associated through behavioral studies to mechanical nociception. We used specific monoclonal antibodies in mice to show that TRAAK is localized exclusively to nodes of Ranvier, the action potential propagating elements of myelinated nerve fibers. Approximately 80 percent of myelinated nerve fibers throughout the central and peripheral nervous system contain TRAAK in an all-nodes or no-nodes per axon fashion. TRAAK is not observed at the axon initial segment where action potentials are first generated. We used polyclonal antibodies, the TRAAK inhibitor RU2 and node clamp amplifiers to demonstrate the presence and functional properties of TRAAK in rat nerve fibers. TRAAK contributes to the ‘leak’ K+ current in mammalian nerve fiber conduction by hyperpolarizing the resting membrane potential, thereby increasing Na+ channel availability for action potential propagation. Mechanical gating in TRAAK might serve a neuroprotective role by counteracting mechanically-induced ectopic action potentials. Alternatively, TRAAK may open in response to mechanical forces in the nodal membrane associated with depolarization during saltatory conduction and thereby contribute to repolarization of the node for subsequent spikes.

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