Extracellular high K+ stimulates vesicular glutamate release from astrocytes by activating voltage‐dependent calcium channels

Authors:
Publisher website
Google Scholar
Abstract
Extracellular high K+ (75 mM) increased intracellular Ca2+ concentrations in cultured rat hippocampal astrocytes, and the Ca2+ rise was abolished by deleting extracellular Ca2+ or cadmium, a non‐selective inhibitor of voltage‐dependent calcium channels (VDCCs). In the reverse transcription‐polymerase chain reaction analysis, cultured astrocytes expressed mRNAs for L type‐VDCC subunits such as α1B, α1C, α1D, and α1E. Extracellular high K+ (75 mM) stimulated glutamate release from astrocytes. The glutamate release was not prevented by the glutamate transporter inhibitor, L‐trans‐pyrrolidine‐2,4‐dicarboxylic acid (PDC), or deleting extracellular Na+, but otherwise it was clearly inhibited by deleting extracellular Ca2+, cadmium, vesicular transport inhibitors such as brefeldin A, bafilomycin A1, and latrunculin B, or botulinum toxin‐A, an exocytosis inhibitor. Extracellular high K+ (75 mM) bleached fluorescent signals of FM1‐43, taken up into the vesicular membrane in astrocytes, that was also inhibited by deleting extracellular Ca2+, cadmium, brefeldin A, bafilomycin A1, latrunculin B, or botulinum toxin‐A, but not by PDC. Taken together, the results of the present study indicate that extracellular high K+‐evoked depolarization activates VDCCs expressed in astrocytes, causing an increase in intracellular Ca2+ concentrations through VDCCs, which triggers vesicular glutamate release from astrocytes, independently of reverse transport through glutamate transporters. J. Cell. Physiol. 225: 512–518, 2010.

This publication has 30 references indexed in Scilit: