Exp Neurobiol 2015; 24(1): 17-23
Published online March 31, 2015
© The Korean Society for Brain and Neural Sciences
Jaekwang Lee1, Ye-Eun Chun1,2, Kyung-Seok Han1, Jungmoo Lee1,3, Dong Ho Woo1 and C. Justin Lee1,2,3*
1Center for Functional Connectomics, and Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul 136-791, 2Neuroscience Program, University of Science and Technology (UST), Daejeon 305-350, 3KU-KIST Graduate School of Converging Science and Technology, Seoul 136-701, Korea
Correspondence to: *To whom correspondence should be addressed.
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Astrocytes and neurons are inseparable partners in the brain. Neurotransmitters released from neurons activate corresponding G protein-coupled receptors (GPCR) expressed in astrocytes, resulting in release of gliotransmitters such as glutamate, D-serine, and ATP. These gliotransmitters in turn influence neuronal excitability and synaptic activities. Among these gliotransmitters, ATP regulates the level of network excitability and is critically involved in sleep homeostasis and astrocytic Ca2+ oscillations. ATP is known to be released from astrocytes by Ca2+-dependent manner. However, the precise source of Ca2+, whether it is Ca2+ entry from outside of cell or from the intracellular store, is still not clear yet. Here, we performed sniffer patch to detect ATP release from astrocyte by using various stimulation. We found that ATP was not released from astrocyte when Ca2+ was released from intracellular stores by activation of Gαq-coupled GPCR including PAR1, P2YR, and B2R. More importantly, mechanical stimulation (MS)-induced ATP release from astrocyte was eliminated when external Ca2+ was omitted. Our results suggest that Ca2+ entry, but not release from intracellular Ca2+ store, is critical for MS-induced ATP release from astrocyte.
Keywords: Astrocytes, ATP, Mechanical stimulation, Ca2+