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

Soo-Jin Oh1, Kyung-Seok Han12, Hyungju Park1, Dong ho Woo12, Hye Yun Kim1, Stephen F Traynelis3 and C Justin Lee12*

Author Affiliations

1 Center for Neural Science and Center for Functional Connectomics, Korea Institute of Science and Technology (KIST), Seoul, South Korea

2 Neuroscience Program, University of Science and Technology (UST), Daejeon, South Korea

3 Department of Pharmacology, School of Medicine, Emory University, Atlanta, GA, USA

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Molecular Brain 2012, 5:38  doi:10.1186/1756-6606-5-38

Published: 12 October 2012



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.


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.


These results provide strong molecular evidence for potential astrocyte-neuron interaction via Best1-mediated glutamate release.

Astrocyte; Bestrophin-1; Glutamate