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Published on: November 26, 2012
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
Summary
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.
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.
