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Author Notes:

Correspondence: C Justin Lee: cjl@kist.re.kr

Authors’ contributions: SJO performed patch clamp recording and wrote the manuscript.

HP and KSH carried out FRET imaging experiments.

DW and HYK performed HPLC analysis.

SFT designed the radioactivity glutamate release assay experiment.

CJL carried out radioactivity glutamate release assay and wrote the manuscript, and supervised entire project.

All authors read and approved the final manuscript.

Disclosures: The authors declare that they have no competing interests.


Research Funding:

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 314-2008-1-C00341).

Protease activated receptor 1-induced glutamate release in cultured astrocytes is mediated by Bestrophin-1 channel but not by vesicular exocytosis


Journal Title:

Molecular Brain


Volume 5, Number 38


, Pages 1-9

Type of Work:

Article | Final Publisher PDF


Background Glutamate is the major transmitter that mediates the principal form of excitatory synaptic transmission in the brain. It has been well established that glutamate is released via Ca2+-dependent exocytosis of glutamate-containing vesicles in neurons. However, whether astrocytes exocytose to release glutamate under physiological condition is still unclear. Findings We report a novel form of glutamate release in astrocytes via the recently characterized Ca2+-activated anion channel, Bestrophin-1 (Best1) by Ca2+ dependent mechanism through the channel pore. We demonstrate that upon activation of protease activated receptor 1 (PAR1), an increase in intracellular Ca2+ concentration leads to an opening of Best1 channels and subsequent release of glutamate in cultured astrocytes. Conclusions These results provide strong molecular evidence for potential astrocyte-neuron interaction via Best1-mediated glutamate release.

Copyright information:

© 2012 Oh et al.; licensee BioMed Central Ltd.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 2.0 Generic License (http://creativecommons.org/licenses/by/2.0/).

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