Investigations on contribution of glial inwardly-rectifying K+ current to membrane potential and ion flux: An experimental and theoretical study

Sheng-Nan Wu, Yan Ming Huang, Ching An Kao, Bing Shuo Chen, Yi Ching Lo

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The inwardly rectifying K+ current [IK(IR)] allows large inward K+ currents at potentials negative to K+ equilibrium potential (EK) and it becomes small outward K+ currents at those positive to EK. How changes of such currents enriched in glial cells can influence the functions of glial cell, neurons, or both is not clearly defined, although mutations of Kir4.1 channels have been demonstrated to cause serious neurological disorders. In this study, we identified the presence of IK(IR) in human glioma cells (U373 and U87 cells). The amplitude of IK(IR) in U373 cells was subject to inhibition by amitriptyline, arecoline, or BaCl2. The activity of inwardly rectifying K+ channels was also clearly detected, and single-channel conductance of these channels was calculated to be around 23 pS. Moreover, based on a simulation model derived from neuron-glial interaction mediated by ion flux, we further found out that incorporation of glial IK(IR) conductance into the model can significantly contribute to regulation of extracellular K+ concentrations and glial resting potential, particularly during high-frequency stimulation. Glial cells and neurons can mutually modulate their expression of ion channels through K+ ions released into the extracellular space. It is thus anticipated that glial IK(IR) may be a potential target utilized to influence the activity of neuronal and glial cells as well as their interaction.

Original languageEnglish
Pages (from-to)9-17
Number of pages9
JournalKaohsiung Journal of Medical Sciences
Volume31
Issue number1
DOIs
Publication statusPublished - 2015 Jan 1

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Neuroglia
Membrane Potentials
Theoretical Models
Ions
Neurons
Arecoline
Inwardly Rectifying Potassium Channel
Amitriptyline
Extracellular Space
Nervous System Diseases
Ion Channels
Glioma
Mutation

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "Investigations on contribution of glial inwardly-rectifying K+ current to membrane potential and ion flux: An experimental and theoretical study",
abstract = "The inwardly rectifying K+ current [IK(IR)] allows large inward K+ currents at potentials negative to K+ equilibrium potential (EK) and it becomes small outward K+ currents at those positive to EK. How changes of such currents enriched in glial cells can influence the functions of glial cell, neurons, or both is not clearly defined, although mutations of Kir4.1 channels have been demonstrated to cause serious neurological disorders. In this study, we identified the presence of IK(IR) in human glioma cells (U373 and U87 cells). The amplitude of IK(IR) in U373 cells was subject to inhibition by amitriptyline, arecoline, or BaCl2. The activity of inwardly rectifying K+ channels was also clearly detected, and single-channel conductance of these channels was calculated to be around 23 pS. Moreover, based on a simulation model derived from neuron-glial interaction mediated by ion flux, we further found out that incorporation of glial IK(IR) conductance into the model can significantly contribute to regulation of extracellular K+ concentrations and glial resting potential, particularly during high-frequency stimulation. Glial cells and neurons can mutually modulate their expression of ion channels through K+ ions released into the extracellular space. It is thus anticipated that glial IK(IR) may be a potential target utilized to influence the activity of neuronal and glial cells as well as their interaction.",
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Investigations on contribution of glial inwardly-rectifying K+ current to membrane potential and ion flux : An experimental and theoretical study. / Wu, Sheng-Nan; Huang, Yan Ming; Kao, Ching An; Chen, Bing Shuo; Lo, Yi Ching.

In: Kaohsiung Journal of Medical Sciences, Vol. 31, No. 1, 01.01.2015, p. 9-17.

Research output: Contribution to journalArticle

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