ArticleSynapse (New York, N.Y.)2009
Phenotypic characterization of mice heterozygous for a null mutation of glutamate carboxypeptidase II.
Article in Synapse (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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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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.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Parallel Metabolomics and Lipidomics of a PSMA/GCPII Deficient Mouse Model Reveal Alteration of NAAG Levels and Brain Lipid Composition.ACS chemical neuroscience · 2024Article
- ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans.Genome biology · 2024Article
- Review
- Mouse glutamate carboxypeptidase II (GCPII) has a similar enzyme activity and inhibition profile but a different tissue distribution to human GCPII.FEBS open bio · 2017Article
- ATP-binding Cassette Subfamily C Member 5 (ABCC5) Functions as an Efflux Transporter of Glutamate Conjugates and Analogs.The Journal of biological chemistry · 2015Article
- Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice: implications for neurodevelopmental disorders.Developmental neurobiology · 2012Article
- Glutamate carboxypeptidase II gene polymorphisms and neural tube defects in a high-risk Chinese population.Metabolic brain disease · 2012Article
- NAAG, NMDA receptor and psychosis.Current medicinal chemistry · 2012Review
- Genetic models of sensorimotor gating: relevance to neuropsychiatric disorders.Current topics in behavioral neurosciences · 2012Review
- Advances in understanding the peptide neurotransmitter NAAG and appearance of a new member of the NAAG neuropeptide family.Journal of neurochemistry · 2011Review
- Deletion of CB2 cannabinoid receptor induces schizophrenia-related behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Discordant behavioral effects of psychotomimetic drugs in mice with altered NMDA receptor function.Psychopharmacology · 2011Article
- Mutant mouse models: genotype-phenotype relationships to negative symptoms in schizophrenia.Schizophrenia bulletin · 2010Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system. Disturbed glutamate signaling resulting in hypofunction of N-methyl-D-aspartate receptors (NMDAR) has been implicated in the pathophysiology of schizophrenia. Glutamate Carboxypeptidase II (GCP II) hydrolyzes N-acetyl-alpha L-aspartyl-L-glutamate (NAAG) into glutamate and N-acetyl-aspartate. NAAG is a neuropeptide that is an NMDAR antagonist as well as an agonist for the metabotropic glutamate receptor-3 (mGluR3), which inhibits glutamate release. The aggregate effect of NAAG is thus to attenuate NMDAR activation. To manipulate the expression of GCP II, LoxP sites were inserted flanking exons 1 and 2, which were excised by crossing with a Cre-expressing mouse. The mice heterozygous for this deletion showed a 50% reduction in the expression level of protein and functional activity of GCP II in brain samples. Heterozygous mutant crosses did not yield any homozygous null animals at birth or as embryos (N > 200 live births and fetuses). These data are consistent with the previous report that GCP II homozygous mutant mice generated by removing exons 9 and 10 of GCP II gene were embryonically lethal and confirm our hypothesis that GCP II plays an essential role early in embryonic development. Heterozygous mice, however, developed normally to adulthood and exhibited increased locomotor activity, reduced social interaction, and a subtle cognitive deficit in working memory.
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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.