Transgenic overexpression of glycine transporter 1 and developmental changes in activity of glycine transporters in mouse central nervous system

Frankfurt (Main), Univ., Diss., 2012

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Bibliographische Detailangaben
1. Verfasser:	Lall, Deepti
Format:	UnknownFormat
Sprache:	eng
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Zusammenfassung:	Frankfurt (Main), Univ., Diss., 2012 Glycine acts as an inhibitory neurotransmitter in many interneurons of the spinal cord and brain stem by activating strychnine-sensitive glycine receptors (GlyRs). In addition, it is an essential co-agonist of glutamate at excitatory N-Methyl-D-Asparate receptors (NMDARs). At both inhibitory and excitatory synapses, the concentration of glycine must be tightly regulated. This is accomplished by two high-affinity Na+-dependent glycine transporters (GlyTs): GlyT1 and GlyT2. GlyT1 is widely expressed in glial cells throughout all major regions of the brain as well as in a subset of glutamatergic neurons, whereas GlyT2 is found only at glycinergic synapses and highly enriched in the plasma membrane of the axonal boutons juxtaposed to GlyRs. Analysis of mice deficient in GlyT1 and GlyT2 has revealed important roles of these transporters during development. Mice deficient in GlyT1 and GlyT2 appear normal at birth but develop complex neuromotor phenotypes that severely shorten the life span of these animals. GlyT1 -/- mice die on the first postnatal day due to a strong overinhibition phenotype. GlyT2 deficient mice are unaffected during the first postnatal week but develop an acute neuromotor disorder thereafter and die around postnatal day 12. Based on the detailed characterization of these knockout mice, GlyT2 has been proposed to be responsible for the reuptake of glycine into glycinergic nerve terminals, whereas GlyT1 is thought to regulate synaptic glycine levels mainly by transporting glycine into surrounding astroglial cells. ...
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