Short-circuiting effects of K+ currents on electrical responses of type-1-like astrocytes from mouse cerebral cortex.
The membrane potential and membrane input resistance of cortical astrocytes from newborn mice were recorded with and without exposure to 1 mM barium. Barium treatment drastically decreased the membrane response to 0 and 35 mM K+. It also revealed an electrogenic component of the Na+,K(+)-ATPase as evident by a biphasic depolarization as a response to ouabain, which was monophasic without barium presence. Untreated mouse astrocytes reacted with small monophasic depolarizations to GABA and glutamate exposure. Barium-treated astrocytes exhibited additional transient responses to both transmitters, similar to those responses of rat astrocytes as found in the literature. The transmitter responses were not changed by exposure to uptake blockers for both transmitter substances. Thus, this electrophysiological study confirms earlier studies with radioactive K+ fluxes in showing that astrocytes derived from mouse brain are capable of short-circuiting electrogenic components and transmitter responses. This extreme high K+ permeability resembles the one reported for endfeet of retinal Muller cells and dissociated astrocytes from optic nerve.
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
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Walz
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Magoski
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology*; D001464:Barium / Q000494:pharmacology*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000502:physiology*; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D010042:Ouabain / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D005971:Glutamates; D015221:Potassium Channels; D001464:Barium; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D010042:Ouabain