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Potassium and the excitability properties of normal human motor axons in vivo.

Boërio D, Bostock H, Spescha R, Z'Graggen WJ - PLoS ONE (2014)

Bottom Line: Hyperkalemia is an important cause of membrane depolarization in renal failure.To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels.This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

ABSTRACT
Hyperkalemia is an important cause of membrane depolarization in renal failure. A recent theoretical model of axonal excitability explains the effects of potassium on threshold electrotonus, but predicts changes in superexcitability in the opposite direction to those observed. To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels. Most threshold electrotonus measures were strongly correlated with potassium, and superexcitability decreased at higher potassium levels (P = 0.016), contrary to the existing model. Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro. This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure. These results demonstrate the importance of taking potassium levels into account when assessing axonal membrane dysfunction by excitability testing, and provide evidence that potassium currents are activated by external potassium in vivo.

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Multiple excitability measurements recorded from normal subjects: motor axons in the median nerve were tested at the wrist and compound muscle action potentials recorded from the abductor pollicis brevis muscle.A–C: Mean +/− SD for all 38 subjects. D–F: Comparisons between means of Lower K (grey) and Higher K (black) groups. A, D: Threshold electrotonus, i.e., threshold changes during and after polarizing currents set to +40 (top), +20, −20 and −40% (bottom) of threshold. B, E: Recovery cycle showing successive phases of refractoriness, superexcitability, and late subexcitability. C,F: Current-threshold (I/V) relationship.
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pone-0098262-g001: Multiple excitability measurements recorded from normal subjects: motor axons in the median nerve were tested at the wrist and compound muscle action potentials recorded from the abductor pollicis brevis muscle.A–C: Mean +/− SD for all 38 subjects. D–F: Comparisons between means of Lower K (grey) and Higher K (black) groups. A, D: Threshold electrotonus, i.e., threshold changes during and after polarizing currents set to +40 (top), +20, −20 and −40% (bottom) of threshold. B, E: Recovery cycle showing successive phases of refractoriness, superexcitability, and late subexcitability. C,F: Current-threshold (I/V) relationship.

Mentions: Nerve excitability waveforms recorded from the median motor nerve are illustrated in Figure 1 for the 38 subjects. In the top row are plotted the mean waveforms for the 38 subjects ±1 SD. These recordings are very similar to previously published normal median/APB recordings [2]. In the bottom row the mean recordings from the Lower K group are compared with those from the Higher K group. Conventional excitability measurements derived from the waveforms are listed in Table 1, with their correlation to the serum potassium values. As previously reported by Kuwabara and colleagues [18], there was a significant tendency for axons to become less superexcitable at higher potassium levels (R = 0.39, P = 0.016). There was a clear tendency for electrotonus to ‘fan in’ at higher potassium levels (i.e. TEd values to decrease, TEh values to increase, Table 1 and Figure 2). Over this limited potassium range, there was no significant dependence of rheobase or strength-duration time constant on potassium.


Potassium and the excitability properties of normal human motor axons in vivo.

Boërio D, Bostock H, Spescha R, Z'Graggen WJ - PLoS ONE (2014)

Multiple excitability measurements recorded from normal subjects: motor axons in the median nerve were tested at the wrist and compound muscle action potentials recorded from the abductor pollicis brevis muscle.A–C: Mean +/− SD for all 38 subjects. D–F: Comparisons between means of Lower K (grey) and Higher K (black) groups. A, D: Threshold electrotonus, i.e., threshold changes during and after polarizing currents set to +40 (top), +20, −20 and −40% (bottom) of threshold. B, E: Recovery cycle showing successive phases of refractoriness, superexcitability, and late subexcitability. C,F: Current-threshold (I/V) relationship.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4043986&req=5

pone-0098262-g001: Multiple excitability measurements recorded from normal subjects: motor axons in the median nerve were tested at the wrist and compound muscle action potentials recorded from the abductor pollicis brevis muscle.A–C: Mean +/− SD for all 38 subjects. D–F: Comparisons between means of Lower K (grey) and Higher K (black) groups. A, D: Threshold electrotonus, i.e., threshold changes during and after polarizing currents set to +40 (top), +20, −20 and −40% (bottom) of threshold. B, E: Recovery cycle showing successive phases of refractoriness, superexcitability, and late subexcitability. C,F: Current-threshold (I/V) relationship.
Mentions: Nerve excitability waveforms recorded from the median motor nerve are illustrated in Figure 1 for the 38 subjects. In the top row are plotted the mean waveforms for the 38 subjects ±1 SD. These recordings are very similar to previously published normal median/APB recordings [2]. In the bottom row the mean recordings from the Lower K group are compared with those from the Higher K group. Conventional excitability measurements derived from the waveforms are listed in Table 1, with their correlation to the serum potassium values. As previously reported by Kuwabara and colleagues [18], there was a significant tendency for axons to become less superexcitable at higher potassium levels (R = 0.39, P = 0.016). There was a clear tendency for electrotonus to ‘fan in’ at higher potassium levels (i.e. TEd values to decrease, TEh values to increase, Table 1 and Figure 2). Over this limited potassium range, there was no significant dependence of rheobase or strength-duration time constant on potassium.

Bottom Line: Hyperkalemia is an important cause of membrane depolarization in renal failure.To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels.This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

ABSTRACT
Hyperkalemia is an important cause of membrane depolarization in renal failure. A recent theoretical model of axonal excitability explains the effects of potassium on threshold electrotonus, but predicts changes in superexcitability in the opposite direction to those observed. To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels. Most threshold electrotonus measures were strongly correlated with potassium, and superexcitability decreased at higher potassium levels (P = 0.016), contrary to the existing model. Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro. This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure. These results demonstrate the importance of taking potassium levels into account when assessing axonal membrane dysfunction by excitability testing, and provide evidence that potassium currents are activated by external potassium in vivo.

Show MeSH
Related in: MedlinePlus