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- W2104613739 abstract "The recent discovery of glycine transporters in both the central nervous system and the periphery suggests that glycine transport may be critical to N -methyl- d -aspartate receptor (NMDAR) function by controlling glycine concentration at the NMDAR modulatory glycine site. Data obtained from whole-cell patch–clamp recordings of hippocampal pyramidal neurons, in vitro , demonstrated that exogenous glycine and glycine transporter type 1 (GLYT1) antagonist selectively enhanced the amplitude of the NMDA component of a glutamatergic excitatory postsynaptic current. The effect was blocked by 2-amino-5-phosphonovaleric acid and 7-chloro-kynurenic acid but not by strychnine. Thus, the glycine-binding site was not saturated under the control conditions. Furthermore, GLYT1 antagonist enhanced NMDAR function during perfusion with medium containing 10 μM glycine, a concentration similar to that in the cerebrospinal fluid in vivo , thereby supporting the hypothesis that the GLYT1 maintains subsaturating concentration of glycine at synaptically activated NMDAR. The enhancement of NMDAR function by specific GLYT1 antagonism may be a feasible target for therapeutic agents directed toward diseases related to hypofunction of NMDAR." @default.
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- W2104613739 date "1998-12-22" @default.
- W2104613739 modified "2023-10-03" @default.
- W2104613739 title "Modulation of <i>N</i> -methyl- <scp>d</scp> -aspartate receptor function by glycine transport" @default.
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- W2104613739 doi "https://doi.org/10.1073/pnas.95.26.15730" @default.
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