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Glycine release from astrocytes via functional reversal of GlyT1
Author(s) -
Shibasaki Koji,
Hosoi Nobutake,
Kaneko Ryosuke,
Tominaga Makoto,
Yamada Katsuya
Publication year - 2017
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.13741
Subject(s) - glycine , glycine receptor , astrocyte , stimulation , strychnine , transporter , chemistry , microbiology and biotechnology , biophysics , biochemistry , biology , amino acid , neuroscience , central nervous system , gene
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 GlyRα1 and Glyβ‐expressing HEK 293T 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.Cover Image for this issue: doi: 10.1111/jnc.13785 .