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pH-sensitive inwardly rectifying chloride current in cultured rat cortical astrocytes.

J K Makara1, G L Petheö, A Tóth

  • 1Department of Physiology and Laboratory of Cellular and Molecular Physiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.

Glia
|April 3, 2001
PubMed
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Extracellular pH significantly influences astrocyte chloride currents, with acidosis enhancing these currents and alkalosis reducing them. This pH-sensitive chloride current may play a role in regulating astrocyte and interstitial pH.

Area of Science:

  • Neuroscience
  • Cell Physiology
  • Biophysics

Background:

  • Astrocytes play crucial roles in maintaining brain homeostasis.
  • Plasma membrane ion transport is vital for astrocyte function.
  • The influence of extracellular pH on astrocyte chloride currents was not fully understood.

Purpose of the Study:

  • To investigate the effect of extracellular pH on plasma membrane chloride currents in cultured rat cortical astrocytes.
  • To characterize the properties and regulation of this pH-sensitive chloride current.

Main Methods:

  • Whole-cell patch-clamp technique was employed to measure chloride currents.
  • Experiments were conducted using symmetrical high chloride solutions and potassium channel inhibitors.
  • Pharmacological agents were used to identify the properties of the current.

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Main Results:

  • Cultured rat cortical astrocytes exhibit a slowly activating, inwardly rectifying chloride current.
  • This current is inhibited by cadmium, zinc, 9-anthracene-carboxylic acid, and 5-nitro-2-(3-phenylpropylamino)benzoic acid.
  • Extracellular acidosis augmented the chloride current, while alkalosis reduced it, with sensitivity most pronounced between pH 6.9-7.9.

Conclusions:

  • The identified chloride current is pH-sensitive and present in astrocytes without specific stimulation.
  • Its properties are similar to cAMP-induced currents but are constitutively expressed.
  • This current may be involved in the regulation of interstitial and astrocyte pH, potentially via carbonic anhydrase and Cl(-)/HCO3(-) antiporter activity.