ReviewCurrent medicinal chemistry2012
NAAG, NMDA receptor and psychosis.
Review in Current medicinal chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- An Emerging Paradigm for ABCC5/MRP5 Function in Human Physiology.International journal of molecular sciences · 2025Review
- The murine ATP-binding cassette transporter C5 (Abcc5/MRP5/cMOAT) plays a role in memory consolidation, circadian rhythm regulation and glutamatergic signalling.Translational psychiatry · 2025Article
- Article
- Dysfunction of the NMDA Receptor in the Pathophysiology of Schizophrenia and/or the Pathomechanisms of Treatment-Resistant Schizophrenia.Biomolecules · 2024Review
- The genie in the bottle-magnified calcium signaling in dorsolateral prefrontal cortex.Molecular psychiatry · 2021Review
- Metabolomic and transcriptomic signatures of prenatal excessive methionine support nature rather than nurture in schizophrenia pathogenesis.Communications biology · 2020Article
- Sleep spindle and slow wave abnormalities in schizophrenia and other psychotic disorders: Recent findings and future directions.Schizophrenia research · 2020Article
- Hippocampal Metabolite Profiles in Two Rat Models of Autism: NMR-Based Metabolomics Studies.Molecular neurobiology · 2020Article
- Dendritic Localization and Exocytosis of NAAG in the Rat Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- The Role of Serine Racemase in the Pathophysiology of Brain Disorders.Advances in pharmacology (San Diego, Calif.) · 2018Review
- Augmentation of Anticancer Drug Efficacy in Murine Hepatocellular Carcinoma Cells by a Peripherally Acting Competitive N-Methyl-d-aspartate (NMDA) Receptor Antagonist.Journal of medicinal chemistry · 2017Article
- BLOC-1 deficiency causes alterations in amino acid profile and in phospholipid and adenosine metabolism in the postnatal mouse hippocampus.Scientific reports · 2017Article
- A Neurophysiological Perspective on a Preventive Treatment against Schizophrenia Using Transcranial Electric Stimulation of the Corticothalamic Pathway.Brain sciences · 2017Review
- Reduced sleep spindle activity point to a TRN-MD thalamus-PFC circuit dysfunction in schizophrenia.Schizophrenia research · 2017Review
- Substance Use Disorders and Schizophrenia.Focus (American Psychiatric Publishing) · 2016Article
- The NMDA Receptor and Schizophrenia: From Pathophysiology to Treatment.Advances in pharmacology (San Diego, Calif.) · 2016Review
- ATP-binding Cassette Subfamily C Member 5 (ABCC5) Functions as an Efflux Transporter of Glutamate Conjugates and Analogs.The Journal of biological chemistry · 2015Article
- In vivo assessment of neurotransmitters and modulators with magnetic resonance spectroscopy: application to schizophrenia.Neuroscience and biobehavioral reviews · 2015Review
- Mutant disrupted-in-schizophrenia 1 in astrocytes: focus on glutamate metabolism.Journal of neuroscience research · 2014Article
- Abnormal partitioning of hexokinase 1 suggests disruption of a glutamate transport protein complex in schizophrenia.Schizophrenia research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
At central synapses, glutamate is the main excitatory neurotransmitter. Once released from presynaptic terminals, glutamate activates a number of different glutamatergic receptors one of which is the ligand gated ionophore glutamatergic subtype N-methyl-D-aspartate receptors (NMDARs). NMDARs play a crucial role in controlling various determinants of synaptic function. N-acetylaspartylglutamate (NAAG) is the most prevalent peptide transmitter in the mammalian central nervous system. NAAG is released upon neuronal depolarization by a calcium-dependent process from glutamatergic and GABAergic neurons. It is cleaved by a specific peptidase located on astrocytes, glutamate carboxypeptidase type II (GCP-II), to N-acetylaspartate (NAA) and glutamate. Current evidence supports the hypothesis that NAAG is an endogenous agonist at G protein coupled mGluR3 receptors and an antagonist at NMDAR. In several disorders and animal models of human diseases, the levels of NAAG and the activity of GCP-II are altered in ways that are consistent with NAAG's role in regulation of glutamatergic neurotransmission. Several lines of evidence suggest that a dysfunction in glutamatergic via the NMDAR might be involved in schizophrenia. This hypothesis has evolved from findings that NMDAR antagonists such as phencyclidine (PCP or "angel dust"), produces a syndrome in normal individuals that closely resembles schizophrenia and exacerbates psychotic symptoms in patients with chronic schizophrenia. Recent postmortem, metabolic and genetic studies have provided evidence that hypofunction of discrete populations of NMDAR can contribute to the symptoms of schizophrenia, at least in some patients. The review outlines the role of endogenous NAAG at NMDAR neurotransmission and its putative role in the pathophysiology of schizophrenia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.