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• W1899972940 abstract "In the mammalian central nervous system, transporter-mediated reuptake may be critical for terminating the neurotransmitter action of d-serine at the strychnine insensitive glycine site of the NMDA receptor. The Na+ independent amino acid transporter alanine–serine–cysteine transporter 1 (Asc-1) has been proposed to account for synaptosomal d-serine uptake by virtue of its high affinity for d-serine and widespread neuronal expression throughout the brain. Here, we sought to validate the contribution of Asc-1 to d-serine uptake in mouse brain synaptosomes using Asc-1 gene knockout (KO) mice. Total [3H]d-serine uptake in forebrain and cerebellar synaptosomes from Asc-1 knockout mice was reduced to 34 ± 5% and 22 ± 3% of that observed in wildtype (WT) mice, respectively. When the Na+ dependent transport components were removed by omission of Na+ ions in the assay buffer, d-serine uptake in knockout mice was reduced to 8 ± 1% and 3 ± 1% of that measured in wildtype mice in forebrain and cerebellum, respectively, suggesting Asc-1 plays a major role in the Na+ independent transport of d-serine. Potency determination of d-serine uptake showed that Asc-1 mediated rapid high affinity Na+ independent uptake with an IC50 of 19 ± 1 µm. The remaining uptake was mediated predominantly via a low affinity Na+ dependent transporter with an IC50 of 670 ± 300 µm that we propose is the glial alanine–serine–cysteine transporter 2 (ASCT2) transporter. The results presented reveal that Asc-1 is the only high affinity d-serine transporter in the mouse CNS and is the predominant mechanism for d-serine reuptake." @default.
• W1899972940 created "2016-06-24" @default.
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• W1899972940 date "2007-04-10" @default.
• W1899972940 modified "2023-10-14" @default.
• W1899972940 title "Evidence from gene knockout studies implicates Asc-1 as the primary transporter mediating d-serine reuptake in the mouse CNS" @default.
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• W1899972940 doi "https://doi.org/10.1111/j.1460-9568.2007.05446.x" @default.
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