Strength-duration properties and their voltage dependence as measures of a threshold conductance at the node of Ranvier of single motor axons

Mogyoros, Ilona; Lin, Cindy S.‐Y.; Kuwabara, Satoshi; Cappelen‐Smith, Cecilia; Burke, David

doi:10.1002/1097-4598(200011)23:11<1719::aid-mus8>3.0.co;2-w

Cited by 19 publications

(13 citation statements)

References 23 publications

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“…Increasing the stimulus pulse width used for NMES caused a greater depression of the M‐wave relative to single stimuli, thus fewer motor axons must have been recruited. Because Na + channels are the major determinant of threshold in axons,39 the depression of M‐waves during NMES is likely related to the inactivation of voltage‐gated Na + channels. The wider pulse widths may have increased the inactivation of voltage‐gated Na + channels in motor axons, as the inactivation time constant of classic fast voltage‐gated Na + channels is 500–1000 μs 40, 41.…”

Section: Discussionmentioning

confidence: 99%

Influence of stimulus pulse width on M‐waves, H‐reflexes, and torque during tetanic low‐intensity neuromuscular stimulation

Lagerquist

Collins

2010

Muscle and Nerve

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Neuromuscular electrical stimulation (NMES) has been shown to generate contractions that include a central recruitment of motoneurons; however, the effect of pulse width on electromyographic (EMG) and torque responses during NMES are not well documented. Soleus EMG and isometric plantarflexion torque were recorded from 14 subjects with NMES delivered to the tibial nerve using 50, 200, 500, and 1000 μs pulse widths. M-waves were significantly smaller during 20 Hz NMES compared with responses evoked by single pulses of 200, 500, and 1000 μs, but not 50 μs pulse widths. At all pulse widths, stimulation at 20 Hz depressed soleus H-reflexes compared with single pulses. Two seconds of 100 Hz NMES significantly increased H-reflexes and torque during the subsequent 20 Hz NMES with 200, 500, and 1000 μs, but not 50 μs, pulse widths. NMES delivered using wide pulses generated larger contractions with a relatively greater central contribution than narrow pulses. This may help reduce atrophy and produce fatigue-resistant contractions for rehabilitation.

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Section: Discussionmentioning

confidence: 99%

Influence of stimulus pulse width on M‐waves, H‐reflexes, and torque during tetanic low‐intensity neuromuscular stimulation

Lagerquist

Collins

2010

Muscle and Nerve

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“…The strength–duration properties, reflecting primarily the function of nodal membrane (Mogyoros et al . , ), were determined by measuring the thresholds for test stimuli with duration of 0.2 to 1 ms. Rheobase (Fig. F ) and the strength–duration time constant (SDTC, Fig.…”

Section: Methodsmentioning

confidence: 99%

Transient impairment of the axolemma following regional anaesthesia by lidocaine in humans

Moldovan

Lange

Aachmann-Andersen

et al. 2014

The Journal of Physiology

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Key pointsr We tested the recovery of motor axon conduction and multiple measures of excitability by 'threshold-tracking' after ultrasound-guided distal median nerve regional anaesthesia by lidocaine.r Lidocaine caused a transient conduction failure that recovered completely by 3 h, whereas excitability recovered only partially by 6 h and fully by 24 h.r The up to 7-fold increase in threshold after complete recovery of conduction was associated with excitability changes that could only partially be explained by block of the voltage-gated Na + channel (VGSC).r Mathematical modelling indicated that, apart from a reduction in the number of functioning VGSCs, lidocaine also caused a decrease of passive membrane resistance and an increase of capacitance.r Our data suggest that lidocaine, even at clinical 'sub-blocking' concentrations, could cause a reversible structural impairment of the axolemma. AbstractThe local anaesthetic lidocaine is known to block voltage-gated Na + channels (VGSCs), although at high concentration it was also reported to block other ion channel currents as well as to alter lipid membranes. The aim of this study was to investigate whether the clinical regional anaesthetic action of lidocaine could be accounted for solely by the block of VGSCs or whether other mechanisms are also relevant. We tested the recovery of motor axon conduction and multiple measures of excitability by 'threshold-tracking' after ultrasound-guided distal median nerve regional anaesthesia in 13 healthy volunteers. Lidocaine caused rapid complete motor axon conduction block localized at the wrist. Within 3 h, the force of the abductor pollicis brevis muscle and median motor nerve conduction studies returned to normal. In contrast, the excitability of the motor axons at the wrist remained markedly impaired as indicated by a 7-fold shift of the stimulus-response curves to higher currents with partial recovery by 6 h and full recovery by 24 h. The strength-duration properties were abnormal with markedly increased rheobase and reduced strength-duration time constant. The changes in threshold during electrotonus, especially during depolarization, were markedly reduced. The recovery cycle showed increased refractoriness and reduced superexcitability. The excitability changes were only partly similar to those previously observed after poisoning with the VGSC blocker tetrodotoxin. Assuming an unaltered ion-channel gating, modelling indicated that, apart from up to a 4-fold reduction in the number of functioning VGSCs, lidocaine also caused a decrease of passive membrane resistance and an increase of capacitance. Our data suggest that the lidocaine effects, even at clinical 'sub-blocking' concentrations, could reflect, at least in part, a reversible structural impairment of the axolemma.

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“…Subsequently, other studies have been conducted on human single motor axons, including the responses to subthreshold polarizing currents (Bostock & Baker, 1988), ectopic behaviour following release of ischaemia (Bostock et al . 1991 a , b ), repetitive activity after tetanic stimulation (Bostock & Bergmans, 1994), strength–duration properties (Mogyoros et al . 2000), threshold variability (Hales et al .…”

Section: Introductionmentioning

confidence: 99%

“…He described the recovery of the excitability of axons following single and repetitive activation and reported the effects of ischaemia and temperature on these processes. Subsequently, other studies have been conducted on human single motor axons, including the responses to subthreshold polarizing currents (Bostock & Baker, 1988), ectopic behaviour following release of ischaemia (Bostock et al 1991a,b), repetitive activity after tetanic stimulation (Bostock & Bergmans, 1994), strength-duration properties (Mogyoros et al 2000), threshold variability (Hales et al 2004) and responses to near-threshold stimuli . However, presumably because of the difficulty of isolating and J Physiol 588.13 tracking single motor axons for extended periods, most studies of axonal excitability in vivo have been conducted using threshold tracking of compound potentials (Bostock et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Properties of low‐threshold motor axons in the human median nerve

Trevillion

Howells

Bostock

et al. 2010

The Journal of Physiology

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This study investigated the excitability and accommodative properties of low-threshold human motor axons to test whether these motor axons have greater expression of the persistent Na + conductance, I NaP . Computer-controlled threshold tracking was used to study 22 single motor units and the data were compared with compound motor potentials of various amplitudes recorded in the same experimental session. Detailed comparisons were made between the single units and compound potentials that were 40% or 5% of maximal amplitude, the former because this is the compound potential size used in most threshold tracking studies of axonal excitability, the latter because this is the compound potential most likely to be composed entirely of motor axons with low thresholds to electrical recruitment. Measurements were made of the strength-duration relationship, threshold electrotonus, current-voltage relationship, recovery cycle and latent addition. The findings did not support a difference in I NaP . Instead they pointed to greater activity of the hyperpolarization-activated inwardly rectifying current (I h ) as the basis for low threshold to electrical recruitment in human motor axons. Computer modelling confirmed this finding, with a doubling of the hyperpolarization-activated conductance proving the best single parameter adjustment to fit the experimental data. We suggest that the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel(s) expressed on human motor axons may be active at rest and contribute to resting membrane potential.

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Strength-duration properties and their voltage dependence as measures of a threshold conductance at the node of Ranvier of single motor axons

Cited by 19 publications

References 23 publications

Influence of stimulus pulse width on M‐waves, H‐reflexes, and torque during tetanic low‐intensity neuromuscular stimulation

Influence of stimulus pulse width on M‐waves, H‐reflexes, and torque during tetanic low‐intensity neuromuscular stimulation

Transient impairment of the axolemma following regional anaesthesia by lidocaine in humans

Properties of low‐threshold motor axons in the human median nerve

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