期刊
JOURNAL OF NEUROCHEMISTRY
卷 140, 期 3, 页码 395-403出版社
WILEY
DOI: 10.1111/jnc.13741
关键词
astrocyte; glycine; glia; gliotransmitter; GlyT1
资金
- Japanese Ministry of Education, Culture, Sports, Science, and Technology [15H05934, 21200012, 20399554, 24111507, 26111702, 26117502, 15H03000, 17590182, 18077012]
- Uehara Memorial Foundation
- Takeda Science Foundation, Tokyo, Japan
- Sumitomo Foundation
- Brain Science Foundation
- Narishige Neuroscience Research Foundation
- Salt Science Research Foundation [14C2]
- Ichiro Kanehara Foundation
- Grants-in-Aid for Scientific Research [15H05934, 26111702, 24111507, 17590182, 16H05438, 18077012, 15KK0331, 15K06696, 26117502, 21200012, 15H03000] Funding Source: KAKEN
It was previously reported that functional glycine receptors were expressed in neonatal prefrontal cortex; however, the glycine-releasing cells were unknown. We hypothesized that astrocytes might be a major glycine source, and examined the glycine release properties of astrocytes. We also hypothesized that dopamine (DA) might be a trigger for the astrocytic glycine release, as numerous DA terminals localize in the cortex. We combined two different methods to confirm the glycine release from astrocytes. Firstly, we analyzed the supernatant of astrocytes by amino acid analyzer after DA stimulation, and detect significant glycine peak. Furthermore, we utilized a patch-clamp biosensor method to confirm the glycine release from astrocytes by using GlyR1 and Gly-expressing HEK293T cells, and detected significant glycine-evoked current upon DA stimulation. Thus, we clearly demonstrated that DA induces glycine release from astrocytes. Surprisingly, DA caused a functional reversal of astrocytic glycine transporter 1, an astrocytic type of glycine transporter, causing astrocytes to release glycine. Hence, astrocytes transduce pre-synaptic DA signals to glycine signals through a reversal of astrocytic glycine transporter 1 to regulate neuronal excitability.
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