ArticleCNS neuroscience & therapeutics2023
Deletion of glutamate carboxypeptidase II (GCPII), but not GCPIII, provided long-term benefits in mice with traumatic brain injury.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Intranasal CRISPR- lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.Research square · 2026Article
- Intranasal CRISPR-lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- Targeting NAAG metabolism restores cognition and synaptic integrity in EcoHIV-infected mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Article
- Single-Cell RNA and Transcriptome Sequencing to Analyze the Role of Lactate Metabolism in Traumatic Brain Injury Astrocytes.Brain and behavior · 2025Article
- GCPII Inhibition Promotes Remyelination after Peripheral Nerve Injury in Aged Mice.International journal of molecular sciences · 2024Article
- Paraventricular thalamus-insular cortex circuit mediates colorectal visceral pain induced by neonatal colonic inflammation in mice.CNS neuroscience & therapeutics · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Effects of radiofrequency field from 5G communication on fecal microbiome and metabolome profiles in mice.Scientific reports · 2024Article
- Deletion of glutamate carboxypeptidase II (GCPII), but not GCPIII, provided long-term benefits in mice with traumatic brain injury.CNS neuroscience & therapeutics · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
main problemN-acetylaspartylglutamate (NAAG) has neuroprotective effects in traumatic brain injury (TBI) by activating metabotropic glutamate receptor 3 (mGluR3) and reducing glutamate release. Glutamate carboxypeptidase II (GCPII) is the primary enzyme responsible for the hydrolysis of NAAG. It remains unclear whether glutamate carboxypeptidase III (GCPIII), a homolog of GCPII, can partially compensate for GCPII's function.
methodsGCPII
resultsIn this study, we found that deletion of GCPII reduced glutamate production, excitotoxicity, and neuronal damage and improved cognitive function, but GCPIII deletion had no significant neuroprotective effect. Additionally, there was no significant difference in the neuroprotective effect between the combination of GCPII and GCPIII deletion and GCPII deletion alone.
conclusionThese results suggest that GCPII inhibition may be a therapeutic option for TBI, and that GCPIII may not act as a complementary enzyme to GCPII in this context.
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Registered trials
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