scholarly journals Outwardly rectifying deflections in threshold electrotonus due to K+conductances

2007 ◽  
Vol 580 (2) ◽  
pp. 685-696 ◽  
Author(s):  
Louise Trevillion ◽  
James Howells ◽  
David Burke
Keyword(s):  
Threshold Electrotonus

scholarly journals Effect of maturation on nerve excitability in an experimental model of threshold electrotonus

2000 ◽  
Vol 23 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Qing Yang ◽  
Ryuji Kaji ◽  
Nobuyuki Hirota ◽  
Yasuhiro Kojima ◽  
Tsunekazu Takagi ◽  
...  
Keyword(s):  
Experimental Model ◽  
Nerve Excitability ◽  
Threshold Electrotonus

Split hand and motor axonal hyperexcitability in spinal and bulbar muscular atrophy

2020 ◽  
Vol 91 (11) ◽  
pp. 1189-1194 ◽  
Author(s):  
Kazumoto Shibuya ◽  
Sonoko Misawa ◽  
Akiyuki Uzawa ◽  
Setsu Sawai ◽  
Atsuko Tsuneyama ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Muscular Atrophy ◽  
Therapeutic Option ◽  
Neuromuscular Diseases ◽  
Cortical Motor ◽  
Peripheral Mechanism ◽  
Compound Muscle Action Potentials ◽  
Axonal Excitability ◽  
Threshold Electrotonus ◽  
Normal Controls

ObjectiveThe ‘split hand’ sign refers to preferential wasting of the thenar and first dorsal interosseous muscles with relatively sparing of the hypothenar muscles in amyotrophic lateral sclerosis (ALS) and both cortical and spinal/peripheral excitotoxic mechanisms have been proposed. We aimed to study split hand and axonal excitability in spinal and bulbar muscular atrophy (SBMA) in which cortical motor neurons are intact.MethodsIn 35 patients with genetically confirmed SBMA, 55 with ALS, 158 with other neuromuscular diseases and 90 normal controls; split hand was strictly determined by amplitudes of compound muscle action potentials. Nerve excitability testing of median motor axons was performed in 35 SBMA and 55 patients with ALS and 45 normal controls.ResultsSplit hand was as frequently found for patients with SBMA (57%) and ALS (62%), compared with disease (20%) and normal (0%) controls. Excitability testing showed that in both SBMA and ALS, strength-duration time constant was longer, and threshold changes in depolarising threshold electrotonus and superexcitability in the recovery cycle were greater than in normal controls (p<0.01).ConclusionsSplit hand is not specific to ALS and can be caused by the peripheral mechanism alone in SBMA, whereas the effect of upper motor neuron lesion cannot be excluded in ALS. Our results also suggest that SBMA and ALS share common axonal excitability changes; increased nodal persistent sodium and reduced potassium currents that may accelerate motor neuronal death and differently affect axons-innervating different muscles. Ion channel modulators could be a therapeutic option for both SBMA and ALS.

Function of the Hyperpolarization-Activated Inward Rectification in Nonmyelinated Peripheral Rat and Human Axons

1997 ◽  
Vol 77 (1) ◽  
pp. 421-426 ◽  
Author(s):  
Peter Grafe ◽  
Stefan Quasthoff ◽  
Julian Grosskreutz ◽  
Christian Alzheimer
Keyword(s):  
Action Potential ◽  
Sural Nerve ◽  
Nerve Fibers ◽  
Stimulation Frequency ◽  
Time Dependent ◽  
Inward Rectification ◽  
Organ Bath ◽  
Vagus Nerves ◽  
Membrane Hyperpolarization ◽  
Threshold Electrotonus

Grafe, Peter, Stefan Quasthoff, Julian Grosskreutz, and Christian Alzheimer. Function of the hyperpolarization-activated inward rectification in nonmyelinated peripheral rat and human axons. J. Neurophysiol. 77: 421–426, 1997. The function of time-dependent, hyperpolarization-activated inward rectification was analyzed on compound potentials of nonmyelinated axons in the mammalian peripheral nervous system. Isolated rat vagus nerves and fascicles of biopsied human sural nerve were tested in a three-chambered, Vaseline-gap organ bath at 37°C. Inward rectification was assessed by recording the effects of long-lasting hyperpolarizing currents on electrical excitability with the use of the method of threshold electrotonus (program QTRAC, copyright Institute of Neurology, London, UK) and by measuring activity-dependent changes in conduction velocity and membrane potential. Prominent time-dependent, cesium-sensitive inward rectification was revealed in rat vagus and human sural nerve by recording threshold electrotonus to 200-ms hyperpolarizing current pulses. A slowing of compound action potential conduction was observed during a gradual increase in the stimulation frequency from 0.1 to 3 Hz. Above a stimulation frequency of 0.3 Hz, this slowing of conduction was enhanced during bath application of 1 mM cesium. Cesium did not alter action potential waveforms during stimulation at frequencies <1 Hz. Cesium-induced slowing in action potential conduction was correlated with membrane hyperpolarization. The hyperpolarization by cesium was stronger during higher stimulation frequencies and small in unstimulated nerves. These data show that a cesium-sensitive, time-dependent inward rectification in peripheral rat and human nonmyelinated nerve fibers limits the slowing in conduction seen in such axons at action potential frequencies higher than ∼0.3 Hz.

scholarly journals Nerve excitability differences in slow and fast motor axons of the rat: more than just Ih

2019 ◽  
Vol 122 (4) ◽  
pp. 1728-1734
Author(s):  
James M. Bell ◽  
Chad Lorenz ◽  
Kelvin E. Jones
Keyword(s):  
Peripheral Nerves ◽  
Motor Axons ◽  
Recovery Cycle ◽  
Nerve Excitability ◽  
Peripheral Nerve Excitability ◽  
Slow Twitch ◽  
Ischemic Depolarization ◽  
Fast Twitch ◽  
Threshold Electrotonus ◽  
Insight Into

The objective was to determine biophysical differences between fast and slow motor axons using threshold tracking and demonstrate confounds related to anesthetic. Nerve excitability of motor axons innervating the slow-twitch soleus (SOL) and fast-twitch tibialis anterior (TA) muscles was tested. The experiments were conducted with pentobarbital sodium (SP) anesthetic and compared with previous results that used ketamine-xylazine (KX). Nerve excitability indices measured with SP show definitive differences between TA and SOL motor axons that extend beyond previous reports. Nerve excitability indices sensitive to changes in Ih indicated an increase in SOL axons compared with TA axons [e.g., S3 t = 7.949 (df = 10), P < 0.001; hyperpolarizing threshold electrotonus (90–100 ms), t = 2.659 (df = 20); P = 0.01; hyperpolarizing I/V slope, t = 4.308 (df = 19); P < 0.001]. SOL axons also had a longer strength-duration time constant [ t = 3.35 (df = 20); P = 0.003] and a longer and larger magnitude relative refractory period [RRP (ms) t = 3.53 (df = 12); P = 0.004; Refractoriness at 2 ms, t = 0.0055 (df = 9); P = 0.006]. Anesthetic choice affected many measures of peripheral nerve excitability with differences most apparent in tests of threshold electrotonus and recovery cycle. For example, recovery cycle with KX lacked a clear superexcitable and late subexcitable period. We conclude that KX had a confounding effect on nerve excitability results consistent with ischemic depolarization. Results using SP revealed the full extent of differences in nerve excitability measures between putative slow and fast motor axons of the rat. These results provide empirical evidence, beyond conduction velocity, that the biophysical properties of motor axons vary with the type of muscle fiber innervated. These differences suggest that fast axons may be predisposed to dysfunction during hyperpolarizing stresses, e.g., electrogenic sodium pumping following sustained impulse conduction. NEW & NOTEWORTHY Nerve excitability testing is a tool used to provide insight into the properties of ion channels in peripheral nerves. It is used clinically to assess pathophysiology of axons. Researchers customarily think of motor axons as homogeneous; however, we demonstrate there are clear differences between fast and slow axons in the rat. This is important for interpreting results with selective motor neuronopathy, like aging where fast axons are at high risk of degeneration.

PS-35-2 Threshold electrotonus in monomelic amyotrophy with spinal hemiatrophy

1995 ◽  
Vol 97 (4) ◽  
pp. S172 ◽  
Author(s):  
Yasuhiro Kojima ◽  
Ryuji Kaji ◽  
Nobuyuki Hirota ◽  
Nobuo Kohara ◽  
Jun Kimura ◽  
...  
Keyword(s):  
Threshold Electrotonus

scholarly journals Axonal excitability and conduction alterations caused by levobupivacaine in rat

2017 ◽  
Vol 67 (3) ◽  
pp. 293-307 ◽  
Author(s):  
Seçkin Tuncer ◽  
Tülay Tuncer Peker ◽  
İlksen Burat ◽  
Erhan Kiziltan ◽  
Barkin İlhan ◽  
...  
Keyword(s):  
Dependent Manner ◽  
Capacitive Properties ◽  
Before And After ◽  
Current Threshold ◽  
Sciatic Nerves ◽  
Axonal Excitability ◽  
Long Acting ◽  
Threshold Electrotonus

Abstract In this study, effects of the long-acting amide-type local anesthetic levobupivacaine on axonal conduction and excitability parameters of the rat sciatic nerve were thoroughly examined both in vitro and in vivo. In order to deduce its effects on isolated nerve conduction, compound nerve action potential (CNAP) recordings were performed using the suction method over sciatic nerves of Wistar rats before and after administration of 0.05 % (1.7 mmol L−1) levobupivacaine. Levobupivacaine caused complete CNAP area and amplitude depression by blocking conduction in a time-dependent manner. To assess the influence of levobupivacaine on in vivo excitability properties, threshold-tracking (TT) protocols were performed at sciatic nerves of rats injected with perineural 0.05 % (1.7 mmol L−1) levobupivacaine or vehicle alone. Charge-duration TT results revealed that levobupivacaine increases the rheobase and decreases the strength-duration time constant, suggesting interference of the anesthetic with the opening of Na+ channels. Twenty and 40 % threshold electrotonus curves were found for both groups to follow the same paths, suggesting no significant effect of levobupivacaine on K+ channels for either the fastest or relatively slow conducting fibers. Current-threshold relationship results revealed no significant effect on axonal rectifying channels. However, according to the results of the recovery cycle protocol yielding the pattern of excitability changes following the impulse, potential deviation was found in the recovery characteristics of Na+ channels from the absolute refractory period. Consequently, conduction blockage caused by levobupivacaine may not be due to the passive (capacitive) properties of axon or the conductance of potassium channels but to the decrease in sodium channel conductance.

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