ArticleSchizophrenia research2009
Localization of NAAG-related gene expression deficits to the anterior hippocampus in schizophrenia.
Article in Schizophrenia research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Expression of group II mGluRs in the inferior colliculus, medial geniculate body, and auditory cortex increases with age.Neuroscience · 2025Article
- Dysfunction of the NMDA Receptor in the Pathophysiology of Schizophrenia and/or the Pathomechanisms of Treatment-Resistant Schizophrenia.Biomolecules · 2024Review
- Excitatory and inhibitory imbalances in the trisynaptic pathway in the hippocampus in schizophrenia: a postmortem ultrastructural study.Journal of neural transmission (Vienna, Austria : 1996) · 2023Article
- D-DOPA Is a Potent, Orally Bioavailable, Allosteric Inhibitor of Glutamate Carboxypeptidase II.Pharmaceutics · 2022Article
- Review
- Reduced Hippocampal Subfield Volume in Schizophrenia and Clinical High-Risk State for Psychosis.Frontiers in psychiatry · 2021Article
- Metabolomic and transcriptomic signatures of prenatal excessive methionine support nature rather than nurture in schizophrenia pathogenesis.Communications biology · 2020Article
- A Role for Phosphodiesterase 11A (PDE11A) in the Formation of Social Memories and the Stabilization of Mood.Advances in neurobiology · 2017Review
- PDE11A regulates social behaviors and is a key mechanism by which social experience sculpts the brain.Neuroscience · 2016Article
- Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies.Neural plasticity · 2016Review
- Magnetic resonance spectroscopy and tissue protein concentrations together suggest lower glutamate signaling in dentate gyrus in schizophrenia.Molecular psychiatry · 2015Article
- In vivo assessment of neurotransmitters and modulators with magnetic resonance spectroscopy: application to schizophrenia.Neuroscience and biobehavioral reviews · 2015Review
- NAAG peptidase inhibitors block cognitive deficit induced by MK-801 and motor activation induced by d-amphetamine in animal models of schizophrenia.Translational psychiatry · 2012Article
- Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice: implications for neurodevelopmental disorders.Developmental neurobiology · 2012Article
- Recent advances in targeting the ionotropic glutamate receptors in treating schizophrenia.Current pharmaceutical biotechnology · 2012Review
- Regional differences in expression of β-tubulin isoforms in schizophrenia.Schizophrenia research · 2012Article
- Glutamatergic synaptic dysregulation in schizophrenia: therapeutic implications.Handbook of experimental pharmacology · 2012Review
- Hippocampal temporal-parietal junction interaction in the production of psychotic symptoms: a framework for understanding the schizophrenic syndrome.Frontiers in human neuroscience · 2012Article
- NAAG, NMDA receptor and psychosis.Current medicinal chemistry · 2012Review
- Targeting glutamate synapses in schizophrenia.Trends in molecular medicine · 2011Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
N-acetyl aspartyl glutamate (NAAG) is an endogenous agonist at the metabotropic glutamate receptor 3 (mGluR3,GRM3) receptor and antagonist at the N-methyl d-aspartate (NMDA) receptor, both receptors important to the pathophysiology of schizophrenia. Glutamate carboxypeptidase II (GCPII), an enzyme that metabolizes NAAG, is also implicated in this illness. In this study, we conducted in situ hybridization experiments to examine expression of mGluR3 and GCPII transcripts along the rostrocaudal axis of the human postmortem hippocampus. We hypothesized that we would find changes in mGluR3 and/or GCPII in the AH but not posterior hippocampus (PH) in schizophrenia. We compared mRNA levels of these genes in the dentate gyrus (DG) and cornu ammonis (CA)1 and CA3 of AH and PH in 20 matched pairs of control and schizophrenia cases. In controls, mGluR3 is highly expressed in the DG and at lower levels in CA1 and CA3 while GCP II is expressed at similar levels in these regions. Group comparisons show a significant reduction of GCPII mRNA level in the AH in schizophrenia. Post hoc analyses reveal this difference is localized to the CA1 region. In addition, we find a significant positive correlation between GCPII and mGluR3 mRNA in the CA3 of the control AH (r=0.66, p=0.008) which is not present in schizophrenia (r=0.096, p=0.76). This may reflect a disrupted functional interaction between NAAG and mGluR3 in CA3 in schizophrenia. These data suggest that NAAG-mediated signaling is disrupted in the AH in schizophrenia and localize the defect to the CA1 and CA3 regions.
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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.