Computer simulations of neuron-glia interactions mediated by ion flux.

Published

Journal Article

Extracellular potassium concentration, [K(+)](o), and intracellular calcium, [Ca(2+)](i), rise during neuron excitation, seizures and spreading depression. Astrocytes probably restrain the rise of K(+) in a way that is only partly understood. To examine the effect of glial K(+) uptake, we used a model neuron equipped with Na(+), K(+), Ca(2+) and Cl(-) conductances, ion pumps and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either "passive", incorporating only leak channels and an ion exchange pump, or it had rectifying K(+) channels. We computed ion fluxes, concentration changes and osmotic volume changes. Increase of [K(+)](o) stimulated the glial uptake by the glial 3Na/2K ion pump. The [K(+)](o) flux through glial leak and rectifier channels was outward as long as the driving potential was outwardly directed, but it turned inward when rising [K(+)](o)/[K(+)](i) ratio reversed the driving potential. Adjustments of glial membrane parameters influenced the neuronal firing patterns, the length of paroxysmal afterdischarge and the ignition point of spreading depression. We conclude that voltage gated K(+) currents can boost the effectiveness of the glial "potassium buffer" and that this buffer function is important even at moderate or low levels of excitation, but especially so in pathological states.

Full Text

Duke Authors

Cited Authors

  • Somjen, GG; Kager, H; Wadman, WJ

Published Date

  • October 2008

Published In

Volume / Issue

  • 25 / 2

Start / End Page

  • 349 - 365

PubMed ID

  • 18297383

Pubmed Central ID

  • 18297383

Electronic International Standard Serial Number (EISSN)

  • 1573-6873

Digital Object Identifier (DOI)

  • 10.1007/s10827-008-0083-9

Language

  • eng

Conference Location

  • United States