Glycine is a coagonist at the NMDA receptor/channel complex

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  • Cited by (174)

    • Modulation of extrasynaptic GABAergic receptor activity influences glutamate release and neuronal survival following excitotoxic damage to mouse spinal cord neurons

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      Citation Excerpt :

      The role of glycine, however, remains more complex. In fact, while this neutral amino acid has long been recognized as an important inhibitory neurotransmitter in the spinal cord (Werman et al., 1968), its action as co-agonist at NMDA receptors (Llano et al., 1988; Thomson, 1990) might actually facilitate glutamate excitotoxicity (Regan and Choi, 1991). Lack of glycine neuroprotection in our experimental model might allude to a balance between its effects pro and against excitotoxicity.

    • Methylphenidate alters monoaminergic and metabolic pathways in the cerebellum of adolescent rats

      2018, European Neuropsychopharmacology
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      In addition, previous studies performed in rodents and primates show co-localisation of glycine with GABA in the cerebellum (Crook et al., 2006; Ottersen et al., 1987), and that both of these amino acid neurotransmitters are released simultaneously (Dugué et al., 2005; Dumoulin et al., 2001). In this respect, glycine is likely to act as a rapid inhibitory neurotransmitter in the brain, which is in contrast with the added effect of this amino acid as a co-agonist with glutamate on excitatory NMDA receptors (Dumoulin et al., 2001; Laube et al., 1993; Nong et al., 2003; Thomson, 1990). Poor motor coordination is a common symptom of ADHD children, and it is possible that the MPH-induced increase of inhibitory amino acid transmitters (i.e. glycine and GABA) together with the decreased cerebellar glutamate levels as recorded in this study, may contribute to the MPH-induced improvement of motor coordination in ADHD (Bart et al., 2013; Fliers et al., 2008).

    • Potential of D-cycloserine in the treatment of behavioral and neuroinflammatory disorders in Parkinson's disease and studies that need to be performed before clinical trials

      2012, Kaohsiung Journal of Medical Sciences
      Citation Excerpt :

      Ligands that can bind include glutamate, glycine and magnesium and zinc ions [97]. Glutamate requires the co-action of glycine to activate NMDA receptors [97,98], and the glycine binding site has been shown to be the main regulatory site of the NMDA receptor [99]. Lack of glycine or exposure to a glycine antagonist results in complete block of the electrophysiological responses of NMDA receptors and can be overcome by supplementation with glycine [100].

    • Alterations in NMDA receptor subunit densities and ligand binding to glycine recognition sites are associated with chronic anxiety in Alzheimer's disease

      2008, Neurobiology of Aging
      Citation Excerpt :

      Therefore, the increased GlyRS binding affinities in these subjects, putatively as a result of NR2A loss, may lead to GlyRS hypersensitivity to endogenous levels of amino acid agonists. Higher GlyRS affinities may also reduce the glycine-sensitive desensitization of NMDA receptors normally observed after receptor activation by glutamate and glycine (Thomson, 1990). Both of these processes may lead to GlyRS hyperfunction and resultant anxiogenic effects.

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    A.M.T. is a Wellcome Trust Lecturer. The advice and contributions sent by many of the authors cited and the help given by Mr P. N. Taylor in preparing the manuscript is gratefully acknowledged.

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