scholarly journals Protein Gelation around Axons Inhibits Action Potential Propagation in Nerve Fibers

2017 ◽  
Vol 07 (04) ◽  
Author(s):  
Wade N Dauberman ◽  
Samuel Breit ◽  
Shaohua Xu
Keyword(s):  
Action Potential ◽  
Nerve Fibers ◽  
Action Potential Propagation ◽  
Protein Gelation

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.

Contribution of auditory nerve fibers to compound action potential of the auditory nerve

2014 ◽  
Vol 112 (5) ◽  
pp. 1025-1039 ◽  
Author(s):  
Jérôme Bourien ◽  
Yong Tang ◽  
Charlène Batrel ◽  
Antoine Huet ◽  
Marc Lenoir ◽  
...  
Keyword(s):  
Action Potential ◽  
Auditory Nerve ◽  
Computational Simulation ◽  
Round Window ◽  
Hearing Threshold ◽  
Compound Action Potential ◽  
Nerve Fibers ◽  
Auditory Nerve Fibers ◽  
Round Window Niche ◽  
Compound Action

Sound-evoked compound action potential (CAP), which captures the synchronous activation of the auditory nerve fibers (ANFs), is commonly used to probe deafness in experimental and clinical settings. All ANFs are believed to contribute to CAP threshold and amplitude: low sound pressure levels activate the high-spontaneous rate (SR) fibers, and increasing levels gradually recruit medium- and then low-SR fibers. In this study, we quantitatively analyze the contribution of the ANFs to CAP 6 days after 30-min infusion of ouabain into the round window niche. Anatomic examination showed a progressive ablation of ANFs following increasing concentration of ouabain. CAP amplitude and threshold plotted against loss of ANFs revealed three ANF pools: 1) a highly ouabain-sensitive pool, which does not participate in either CAP threshold or amplitude, 2) a less sensitive pool, which only encoded CAP amplitude, and 3) a ouabain-resistant pool, required for CAP threshold and amplitude. Remarkably, distribution of the three pools was similar to the SR-based ANF distribution (low-, medium-, and high-SR fibers), suggesting that the low-SR fiber loss leaves the CAP unaffected. Single-unit recordings from the auditory nerve confirmed this hypothesis and further showed that it is due to the delayed and broad first spike latency distribution of low-SR fibers. In addition to unraveling the neural mechanisms that encode CAP, our computational simulation of an assembly of guinea pig ANFs generalizes and extends our experimental findings to different species of mammals. Altogether, our data demonstrate that substantial ANF loss can coexist with normal hearing threshold and even unchanged CAP amplitude.

Presynaptic Afferent Inhibition of Lobster Olfactory Receptor Cells: Reduced Action-Potential Propagation Into Axon Terminals

1998 ◽  
Vol 80 (2) ◽  
pp. 1011-1015 ◽  
Author(s):  
Matt Wachowiak ◽  
Lawrence B. Cohen
Keyword(s):  
Action Potential ◽  
Olfactory Receptor ◽  
Receptor Cell ◽  
Action Potential Propagation ◽  
Cell Axon ◽  
Axon Terminals ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Afferent Inhibition ◽  
Reduced Action

Wachowiak, Matt and Lawrence B. Cohen. Presynaptic afferent inhibition of lobster olfactory receptor cells: reduced action-potential propagation into axon terminals. J. Neurophysiol. 80: 1011–1015, 1998. Action-potential propagation into the axon terminals of olfactory receptor cells was measured with the use of voltage-sensitive dye imaging in the isolated spiny lobster brain. Conditioning shocks to the olfactory nerve, known to cause long-lasting suppression of olfactory lobe neurons, allowed the selective imaging of activity in receptor cell axon terminals. In normal saline the optical signal from axon terminals evoked by a test stimulus was brief (40 ms) and small in amplitude. In the presence of low-Ca2+/high-Mg2+ saline designed to reduce synaptic transmission, the test response was unchanged in time course but increased significantly in amplitude (57 ± 16%, means ± SE). This increase suggests that propagation into receptor cell axon terminals is normally suppressed after a conditioning shock; this suppression is presumably synaptically mediated. Thus our results show that presynaptic inhibition occurs at the first synapse in the olfactory pathway and that the inhibition is mediated, at least in part, via suppression of action-potential propagation into the presynaptic terminal.

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