ArticleHippocampus2012
Synaptic underpinnings of altered hippocampal function in glutaminase-deficient mice during maturation.
Article in Hippocampus, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 20 citations in OpenAlex.
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- Article
- Astrocyte coverage of excitatory synapses correlates to measures of synapse structure and function in primary visual cortex.bioRxiv : the preprint server for biology · 2023Article
- Glial Glutamine Homeostasis in Health and Disease.Neurochemical research · 2023Review
- Glutaminase activity in GLS1 Het mouse brain compared to putative pharmacological inhibition by ebselen using ex vivo MRS.Neurochemistry international · 2019Article
- Molecular Imaging of mGluR5 Availability with [Cellular and molecular neurobiology · 2019Article
- Article
- Using human brain imaging studies as a guide toward animal models of schizophrenia.Neuroscience · 2016Review
- Genetic Pharmacotherapy as an Early CNS Drug Development Strategy: Testing Glutaminase Inhibition for Schizophrenia Treatment in Adult Mice.Frontiers in systems neuroscience · 2015Article
- Therapeutic strategies impacting cancer cell glutamine metabolism.Future medicinal chemistry · 2013Review
- Article
- Modeling resilience to schizophrenia in genetically modified mice: a novel approach to drug discovery.Expert review of neurotherapeutics · 2012Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Glutaminase-deficient mice (GLS1 hets), with reduced glutamate recycling, have a focal reduction in hippocampal activity, mainly in CA1, and manifest behavioral and neurochemical phenotypes suggestive of schizophrenia resilience. To address the basis for the hippocampal hypoactivity, we examined synaptic plastic mechanisms and glutamate receptor expression. Although baseline synaptic strength was unaffected in Schaffer collateral inputs to CA1, we found that long-term potentiation was attenuated. In wild-type (WT) mice, GLS1 gene expression was highest in the hippocampus and cortex, where it was reduced by about 50% in GLS1 hets. In other brain regions with lower WT GLS1 gene expression, there were no genotypic reductions. In adult GLS1 hets, NMDA receptor NR1 subunit gene expression was reduced, but not AMPA receptor GluR1 subunit gene expression. In contrast, juvenile GLS1 hets showed no reductions in NR1 gene expression. In concert with this, adult GLS1 hets showed a deficit in hippocampal-dependent contextual fear conditioning, whereas juvenile GLS1 hets did not. These alterations in glutamatergic synaptic function may partly explain the hippocampal hypoactivity seen in the GLS1 hets. The maturity-onset reduction in NR1 gene expression and in contextual learning supports the premise that glutaminase inhibition in adulthood should prove therapeutic in 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.