Glycine is a coagonist at the NMDA receptor/channel complex
References (172)
- et al.
Blockade of response in enzyme-treated rat hippocampal neurons
Neurosci. Lett.
(1988) - et al.
promotes the survival of cerebellar granule cells: pharmacological characterization
Neurosci. Lett.
(1989) - et al.
Molecular biology of the GABA receptor: the receptor/channel superfamily
TINS
(1987) - et al.
Differential modulation of [3H]TCP binding to the NMDA receptor by l-glutamate and glycine
Eur. J. Pharmac.
(1988) - et al.
Kynurenate and FG9041 have both competitive and non-competitive antagonist actions at excitatory amino acid receptors
Eur. J. Pharmac.
(1988) - et al.
6,7-dinitroquinoxaline-2,3-dion and 6-nitro,7-cyanoquinoxaline-2,3-dion antagonise responses to NMDA in the rat spinal cord via an action at the strychnine-insensitive glycine receptor
Eur. J. Pharmac.
(1988) - et al.
CNQX blocks acidic amino acid induced depolarizations and synaptic components mediated by non-NMDA receptors in rat hippocampal slices
Neurosci. Lett.
(1988) - et al.
NMDA receptor regulation of neuronal morphology in cultured hippocampal neurons
Neurosci. Lett.
(1989) - et al.
Ifenprodil and SL 82.0715 are antagonists at the polyamine site of the (NMDA) receptor
Eur. J. Pharmac.
(1989) - et al.
Glycine action of receptors in rat hippocampal neurons
Neurosci. Lett.
(1989)
NMDA receptors-their role in long-term potentation
TINS
Excitatory amino acids in the brain—focus on NMDA receptors
TINS
Anatomical organization of excitatory amino acid receptors and their pathways
TINS
Patchclamp recording from single glutamate-receptor channels
TIPS
Kynurenate and 2-amino-5-phosphonovalerate interact with multiple binding sites of the glutamate receptor domain
Neurosci. Lett.
Modulation of glutamate receptors by phencyclidine and glycine in the rat cerebellum: cGMP increase in vivo
Brain Res.
2-amino-5-phosphonovalerate (2APV), a potent and selective antagonist of amino acid-induced and synaptic excitation
Neurosci. Lett.
Differences in results from in vivo and in vitro studies on the use-dependency of N-methylaspartate antagonism by MK-801 and other phencyclidine receptor ligands
Eur. J. Pharmac.
Glycine reverses the effect of HA-966[HA-966] on NMDA responses in cultured rat cortical neurons and in chick retina
Neurosci. Lett.
Glycine and d-serine increase the affinity of sensitive glutamate binding sites in rat brain synaptic membranes
Neuropharmacology
Amino acid neurotransmitters and their pathways in the mammalian central nervous system
Neuroscience
Glycine reverses antagonism of (NMDA) by 1-hydroxy-3-aminopyrrolidone-2 (HA-966) but not by d-2-amino-5-phosphonovalerate (D-AP5) on rat cortical slices
Eur. J. Pharmac.
6,7-dichloro-3-hydroxy-2-quinoxalinecarboxylic acid is a relatively potent antagonist at NMDA and kainate receptors
Neurosci. Lett.
Kynurenic acid inhibits synaptic and acidic amino acid induced responses in the rat hippocampus and spinal cord
Brain Res.
Physiological mechanisms underlying long-term potentiation
TINS
Long-term potentiation on the hippocampus involves activation of receptors
Brain Res.
Intracellular demonstration of an receptor mediated component of synaptic transmission in the rat hippocampus
Neurosci. Lett.
d-cycloserine: a ligand for the coupled glycine receptor has partial agonist characteristics
Neurosci. Lett.
1-aminocyclobutane-1-carboxylate (ACBC): a specific antagonist of the receptor coupled glycine receptor
Eur. J. Pharmac.
Equilibrium analysis of [3H]TCP binding effects of glycine, magnesium and agonists
Eur. J. Pharmac.
HA-966 acts at a modulatory glycine site to inhibit neurotransmitter release
Eur. J. Pharmac.
Non-competitive antagonists of excitatory amino acid receptors
TINS
Quinoxaline derivatives are high-affinity antagonists of the NMDA receptor-associated glycines sites
Brain Res.
l-homocysteic acid but not l-glutamate is an endogenous acid receptor preferring agonist in rat neocortical neurones in vitro
Neurosci. Lett.
Activation of receptors contributes to the EPSP at perforant path synapses in the rat dentate gyrus in vitro
Neurosci. Lett.
CGS 19755 [CGS19755] is a potent and competitive antagonist at NMDA-type receptors
Eur. J. Pharmac.
NMDA receptor activation and early olfactory learning
Dev. Brain Res.
The physiology of excitatory amino acids in the vertebrate central nervous system
Prog. Neurobiol.
Cellular mechanisms underlying excitotoxicity
TINS
Effects of new antagonists on synaptic transmission in the in vitro rat hippocampus
J. Physiol.
Long-term potentiation and NMDA receptors in rat visual cortex
Nature
The NMDA receptor, its channel, and its modulation by glycine
Electrophysiological studies of NMDA receptors
TINS
Synaptic facilitation requires paired activation of convergent excitatory pathways in the neocortex
Nature
A kinetic analysis of the modulation of acid receptors by glycine in mouse cultured hippocampal neurones
J. Physiol.
Concentration jump experiments with NMDA antagonists in mouse cultured hippocampal neurons
J. Neurophysiol
Glycine and glutamate regulation of the NMDA receptor-gated ion channel: allosteric interactions
Soc. Neurosci. Abstr.
Glycine binding sites and NMDA receptors in brain
Nature
Light microscopic autoradiographic localization of [3H]glycine and [3H]strychnine binding sites in rat brain
Eur. J. Pharmac.
Polyamine activation of NMDA effector requires occupation by agonists of both glycine and NMDA sites
Soc. Neurosci. Abstr.
Cited by (174)
Modulation of extrasynaptic GABAergic receptor activity influences glutamate release and neuronal survival following excitotoxic damage to mouse spinal cord neurons
2019, Neurochemistry InternationalCitation 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 NeuropsychopharmacologyCitation Excerpt :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 SciencesCitation 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 AgingCitation 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.
Neonatal epilepsy and inborn errors of metabolism
2006, Archives de PediatrieDynamics of forward and reverse transport by the glial glycine transporter, Glyt1b
2005, Biophysical Journal
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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.