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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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Threshold electrotonus (top row) and recovery cycle (bottom row) waveforms generated by Models 1–3 for values of extracellular potassium corresponding to the Lower K (grey) and Higher K (black) groups.
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pone-0098262-g003: Threshold electrotonus (top row) and recovery cycle (bottom row) waveforms generated by Models 1–3 for values of extracellular potassium corresponding to the Lower K (grey) and Higher K (black) groups.

Mentions: Figure 3 shows electrotonus and recovery cycle waveforms generated by the three models for potassium concentrations equal to the Lower K (3.82 mmol/l) and Higher K (4.39 mmol/l) groups, which can be compared with the recordings in Figures 1D and 1E. Only Model 3 shows an increase in superexcitability at lower potassium levels and fanning-out of depolarising as well as hyperpolarising threshold electrotonus as seen in the recordings.


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

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

Threshold electrotonus (top row) and recovery cycle (bottom row) waveforms generated by Models 1–3 for values of extracellular potassium corresponding to the Lower K (grey) and Higher K (black) groups.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098262-g003: Threshold electrotonus (top row) and recovery cycle (bottom row) waveforms generated by Models 1–3 for values of extracellular potassium corresponding to the Lower K (grey) and Higher K (black) groups.
Mentions: Figure 3 shows electrotonus and recovery cycle waveforms generated by the three models for potassium concentrations equal to the Lower K (3.82 mmol/l) and Higher K (4.39 mmol/l) groups, which can be compared with the recordings in Figures 1D and 1E. Only Model 3 shows an increase in superexcitability at lower potassium levels and fanning-out of depolarising as well as hyperpolarising threshold electrotonus as seen in the recordings.

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