Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2016 Oct 19;6:35592. doi: 10.1038/srep35592

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

PMC Copyright notice

Either via direct supply of glycine, or through supply of biosynthetic precursors such as L-serine, astrocytic SLC7A10 mediates the cytoplasmic enrichment of glycine in glycinergic inhibitory neurons required to maintain adequate loading/quantal content of glycinergic synaptic vesicles. This model predicts that Slc7a10-null mice are unable to supply or recycle glycine (or glycine precursors) from astrocytes to glycinergic neurons; insufficient cytoplasmic concentration of glycine within glycinergic neurons leads to decreased vesicular glycine quanta, as reflected in diminished glycinergic mIPSC amplitudes and a hyperekplexia-like phenotype. Our observation that mice heterozygous for Slc7a10 show mIPSC amplitudes intermediate to those of Slc7a10-null mice and wild type mice is consistent with a concentration-dependent model.