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.

Cerebral white matter injury and damage to myelin sheath following whole-brain ischemia

2013 ◽  
Vol 1495 ◽  
pp. 11-17 ◽  
Author(s):  
Yingzhu Chen ◽  
Qiong Yi ◽  
Gang Liu ◽  
Xue Shen ◽  
Lihui Xuan ◽  
...  
Keyword(s):  
White Matter ◽  
Brain Ischemia ◽  
Myelin Sheath ◽  
White Matter Injury ◽  
Cerebral White Matter ◽  
Whole Brain

Dichotomy of Action-Potential Backpropagation in CA1 Pyramidal Neuron Dendrites

2001 ◽  
Vol 86 (6) ◽  
pp. 2998-3010 ◽  
Author(s):  
Nace L. Golding ◽  
William L. Kath ◽  
Nelson Spruston
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Synaptic Activity ◽  
Resting Potential ◽  
Model Parameters ◽  
Voltage Sensitivity ◽  
Whole Cell ◽  
Ca1 Pyramidal Neurons ◽  
Whole Cell Recordings

In hippocampal CA1 pyramidal neurons, action potentials are typically initiated in the axon and backpropagate into the dendrites, shaping the integration of synaptic activity and influencing the induction of synaptic plasticity. Despite previous reports describing action-potential propagation in the proximal apical dendrites, the extent to which action potentials invade the distal dendrites of CA1 pyramidal neurons remains controversial. Using paired somatic and dendritic whole cell recordings, we find that in the dendrites proximal to 280 μm from the soma, single backpropagating action potentials exhibit <50% attenuation from their amplitude in the soma. However, in dendritic recordings distal to 300 μm from the soma, action potentials in most cells backpropagated either strongly (26–42% attenuation; n = 9/20) or weakly (71–87% attenuation; n = 10/20) with only one cell exhibiting an intermediate value (45% attenuation). In experiments combining dual somatic and dendritic whole cell recordings with calcium imaging, the amount of calcium influx triggered by backpropagating action potentials was correlated with the extent of action-potential invasion of the distal dendrites. Quantitative morphometric analyses revealed that the dichotomy in action-potential backpropagation occurred in the presence of only subtle differences in either the diameter of the primary apical dendrite or branching pattern. In addition, action-potential backpropagation was not dependent on a number of electrophysiological parameters (input resistance, resting potential, voltage sensitivity of dendritic spike amplitude). There was, however, a striking correlation of the shape of the action potential at the soma with its amplitude in the dendrite; larger, faster-rising, and narrower somatic action potentials exhibited more attenuation in the distal dendrites (300–410 μm from the soma). Simple compartmental models of CA1 pyramidal neurons revealed that a dichotomy in action-potential backpropagation could be generated in response to subtle manipulations of the distribution of either sodium or potassium channels in the dendrites. Backpropagation efficacy could also be influenced by local alterations in dendritic side branches, but these effects were highly sensitive to model parameters. Based on these findings, we hypothesize that the observed dichotomy in dendritic action-potential amplitude is conferred primarily by differences in the distribution, density, or modulatory state of voltage-gated channels along the somatodendritic axis.

scholarly journals The Myelin Sheath Maintains the Spatiotemporal Fidelity of Action Potentials by Eliminating the Effect of Quantum Tunneling of Potassium Ions through the Closed Channels of the Neuronal Membrane

2019 ◽  
Vol 1 (2) ◽  
pp. 287-294 ◽  
Author(s):  
Abdallah Barjas Qaswal
Keyword(s):  
Potassium Channels ◽  
Action Potential ◽  
Myelin Sheath ◽  
Quantum Tunneling ◽  
Action Potentials ◽  
Quantum Physics ◽  
Demyelinating Diseases ◽  
Neuronal Membrane ◽  
Potassium Ions ◽  
Axonal Membrane

The myelin sheath facilitates action potential conduction along the axons, however, the mechanism by which myelin maintains the spatiotemporal fidelity and limits the hyperexcitability among myelinated neurons requires further investigation. Therefore, in this study, the model of quantum tunneling of potassium ions through the closed channels is used to explore this function of myelin. According to the present calculations, when an unmyelinated neuron fires, there is a probability of 9.15 × 10 − 4 that it will induce an action potential in other unmyelinated neurons, and this probability varies according to the type of channels involved, the channels density in the axonal membrane, and the surface area available for tunneling. The myelin sheath forms a thick barrier that covers the potassium channels and prevents ions from tunneling through them to induce action potential. Hence, it confines the action potentials spatiotemporally and limits the hyperexcitability. On the other hand, lack of myelin, as in unmyelinated neurons or demyelinating diseases, exposes potassium channels to tunneling by potassium ions and induces the action potential. This approach gives different perspectives to look at the interaction between neurons and explains how quantum physics might play a role in the actions occurring in the nervous system.

Computer Model for Action Potential Propagation Through Branch Point in Myelinated Nerves

2001 ◽  
Vol 85 (1) ◽  
pp. 197-210 ◽  
Author(s):  
Lei Zhou ◽  
Shing Yan Chiu
Keyword(s):  
Action Potential ◽  
Branch Point ◽  
Myelin Sheath ◽  
Nerve Fibers ◽  
Myelinated Nerve ◽  
Axonal Membrane ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Action Potential Propagation ◽  
Periaxonal Space

A mathematical model is developed for simulation of action potential propagation through a single branch point of a myelinated nerve fiber with a parent branch bifurcating into two identical daughter branches. This model is based on a previously published multi-layer compartmental model for single unbranched myelinated nerve fibers. Essential modifications were made to couple both daughter branches to the parent branch. There are two major features in this model. First, the model could incorporate detailed geometrical parameters for the myelin sheath and the axon, accomplished by dividing both structures into many segments. Second, each segment has two layers, the myelin sheath and the axonal membrane, allowing voltages of intra-axonal space and periaxonal space to be calculated separately. In this model, K ion concentration in the periaxonal space is dynamically linked to the activity of axonal fast K channels underneath the myelin in the paranodal region. Our model demonstrates that the branch point acts like a low-pass filter, blocking high-frequency transmission from the parent to the daughter branches. Theoretical analysis showed that the cutoff frequency for transmission through the branch point is determined by temperature, local K ion accumulation, width of the periaxonal space, and internodal lengths at the vicinity of the branch point. Our result is consistent with empirical findings of irregular spacing of nodes of Ranvier at axon abors, suggesting that branch points of myelinated axons play important roles in signal integration in an axonal tree.

scholarly journals Modeling noise mechanisms in neuronal synaptic transmission

2017 ◽  
Author(s):  
Abhyudai Singh
Keyword(s):  
Action Potential ◽  
Synaptic Transmission ◽  
Action Potentials ◽  
Spike Timing ◽  
Critical Threshold ◽  
Model Parameters ◽  
Postsynaptic Neuron ◽  
Presynaptic Neuron ◽  
Vesicle Release ◽  
First Time

In the nervous system, communication occurs via synaptic transmission where signaling molecules (neurotransmitters) are released by the presynaptic neuron, and they influence electrical activity of another neuron (postsynaptic neuron). The inherent probabilistic release of neurotransmitters is a significant source of noise that critically impacts the timing of spikes (action potential) in the postsynaptic neuron. We develop a stochastic model that incorporates noise mechanisms in synaptic transmission, such as, random docking of neurotransmitter-filled vesicle to a finite number of docking sites, with each site having a probability of vesicle release upon arrival of an action potential. This random, burst-like release of neurotransmitters serves as an input to an integrate-and-fire model, where spikes in the postsynaptic neuron are triggered when its membrane potential reaches a critical threshold for the first time. We derive novel analytical results for the probability distribution function of spike timing, and systematically investigate how underlying model parameters and noise processes regulate variability in the inter-spike times. Interestingly, in some parameter regimes, independent arrivals of action potentials in the presynaptic neuron generate strong dependencies in the spike timing of the postsynaptic neuron. Finally, we argue that probabilistic release of neurotransmitters is not only a source of disturbance, but plays a beneficial role in synaptic information processing.

scholarly journals An automated method for precise axon reconstruction from recordings of high-density micro-electrode arrays

2021 ◽  
Author(s):  
Alessio Paolo Buccino ◽  
Xinyue Yuan ◽  
Vishalini Emmenegger ◽  
Xiaohan Xue ◽  
Tobias Gaenswein ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Electrical Potential ◽  
Simulated Data ◽  
Signal Propagation ◽  
High Density ◽  
Electrode Arrays ◽  
Action Potential Propagation ◽  
Automated Method ◽  
Propagation Velocities

Neurons communicate with each other by sending action potentials through their axons. The velocity of axonal signal propagation describes how fast electrical action potentials can travel, and can be affected in a human brain by several pathologies, including multiple sclerosis, traumatic brain injury and channelopathies. High-density microelectrode arrays (HD-MEAs) provide unprecedented spatio-temporal resolution to extracellularly record neural electrical activity. The high density of the recording electrodes enables to image the activity of individual neurons down to subcellular resolution, which includes the propagation of axonal signals. However, axon reconstruction, to date, mainly relies on a manual approach to select the electrodes and channels that seemingly record the signals along a specific axon, while an automated approach to track multiple axonal branches in extracellular action-potential recordings is still missing. In this article, we propose a fully automated approach to reconstruct axons from extracellular electrical-potential landscapes, so-called "electrical footprints" of neurons. After an initial electrode and channel selection, the proposed method first constructs a graph, based on the voltage signal amplitudes and latencies. Then, the graph is interrogated to extract possible axonal branches. Finally, the axonal branches are pruned and axonal action-potential propagation velocities are computed. We first validate our method using simulated data from detailed reconstructions of neurons, showing that our approach is capable of accurately reconstructing axonal branches. We then apply the reconstruction algorithm to experimental recordings of HD-MEAs and show that it can be used to determine axonal morphologies and signal-propagation velocities at high throughput. We introduce a fully automated method to reconstruct axonal branches and estimate axonal action-potential propagation velocities using HD-MEA recordings. Our method yields highly reliable and reproducible velocity estimations, which constitute an important electrophysiological feature of neuronal preparations.

scholarly journals Recording action potential propagation in single axons using multi-electrode arrays

2017 ◽  
Author(s):  
Kenneth R. Tovar ◽  
Daniel C. Bridges ◽  
Bian Wu ◽  
Connor Randall ◽  
Morgane Audouard ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Action Potential ◽  
Sodium Channels ◽  
Action Potentials ◽  
Extracellular Recording ◽  
Electrode Arrays ◽  
Action Potential Propagation ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Axonal Arbors

AbstractThe small caliber of central nervous system (CNS) axons makes routine study of axonal physiology relatively difficult. However, while recording extracellular action potentials from neurons cultured on planer multi-electrode arrays (MEAs) we found activity among groups of electrodes consistent with action potential propagation in single neurons. Action potential propagation was evident as widespread, repetitive cooccurrence of extracellular action potentials (eAPs) among groups of electrodes. These eAPs occurred with invariant sequences and inter-electrode latencies that were consistent with reported measures of action potential propagation in unmyelinated axons. Within co-active electrode groups, the inter-electrode eAP latencies were temperature sensitive, as expected for action potential propagation. Our data are consistent with these signals primarily reflecting axonal action potential propagation, from axons with a high density of voltage-gated sodium channels. Repeated codetection of eAPs by multiple electrodes confirmed these eAPs are from individual neurons and averaging these eAPs revealed sub-threshold events at other electrodes. The sequence of electrodes at which eAPs co-occur uniquely identifies these neurons, allowing us to monitor spiking of single identified neurons within neuronal ensembles. We recorded dynamic changes in single axon physiology such as simultaneous increases and decreases in excitability in different portions of single axonal arbors over several hours. Over several weeks, we measured changes in inter-electrode propagation latencies and ongoing changes in excitability in different regions of single axonal arbors. We recorded action potential propagation signals in human induced pluripotent stem cell-derived neurons which could thus be used to study axonal physiology in human disease models.Significance StatementStudying the physiology of central nervous system axons is limited by the technical challenges of recording from axons with pairs of patch or extracellular electrodes at two places along single axons. We studied action potential propagation in single axonal arbors with extracellular recording with multi-electrode arrays. These recordings were non-invasive and were done from several sites of small caliber axons and branches. Unlike conventional extracellular recording, we unambiguously identified and labelled the neuronal source of propagating action potentials. We manipulated and quantified action potential propagation and found a surprisingly high density of axonal voltage-gated sodium channels. Our experiments also demonstrate that the excitability of different portions of axonal arbors can be independently regulated on time scales from hours to weeks.

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.

Images of Action Potential Propagation in Heart

Physiology ◽  
2000 ◽  
Vol 15 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Guy Salama ◽  
Bum-Rak Choi
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Imaging Techniques ◽  
Three Dimensional ◽  
Fiber Structure ◽  
Intercellular Coupling ◽  
Av Node ◽  
Action Potential Propagation ◽  
Voltage Sensitive Dyes

Activation and repolarization across mammalian hearts follow complex three-dimensional pathways that are governed by fiber structure, intercellular coupling, and action potentials (APs) with spatially heterogeneous properties. Voltage-sensitive dyes and imaging techniques offer new insights on how spatiotemporal heterogeneities of APs govern propagation, repolarization, and AV node conduction and help us visualize arrhythmias with previously unattainable details.

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