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Glial glycine transporter 1 function is essential for early postnatal survival but dispensable in adult mice
Author(s) -
Eulenburg Volker,
Retiounskaia Marina,
Papadopoulos Theofilos,
Gomeza Jesús,
Betz Heinrich
Publication year - 2010
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20987
Subject(s) - biology , transporter , glycine , neuroscience , function (biology) , microbiology and biotechnology , genetics , gene , amino acid
The glycine transporter 1 (GlyT1) is expressed in astrocytes and selected neurons of the mammalian CNS. In newborn mice, GlyT1 is crucial for efficient termination of glycine‐mediated inhibitory neurotransmission. Furthermore, GlyT1 has been implicated in the regulation of excitatory N‐methyl‐D‐asparate (NMDA) receptors. To evaluate whether glial and neuronal GlyT1 have distinct roles at inhibitory synapses, we inactivated the GlyT1 gene cell type‐specifically using mice carrying floxed GlyT1 alleles GlyT1 (+)/+) . GlyT1 (+)/(+) mice expressing Cre recombinase in glial cells developed severe neuromotor deficits during the first postnatal week, which mimicked the phenotype of conventional GlyT1 knock‐out mice and are consistent with glycinergic over‐inhibition. In contrast, Cre‐mediated inactivation of the GlyT1 gene in neuronal cells did not result in detectable motor impairment. Notably, some animals deficient for glial GlyT1 survived the first postnatal week and did not develop neuromotor deficits throughout adulthood, although GlyT1 expression was efficiently reduced. Thus, glial GlyT1 is critical for the regulation of glycine levels at inhibitory synapses only during early postnatal life. © 2010 Wiley‐Liss, Inc.