ArticlePloS one2012
Deletion of glutamate delta-1 receptor in mouse leads to aberrant emotional and social behaviors.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 119 citations in OpenAlex.
- Genetic mutations and synaptic dysfunctions in social interaction disorders: insights from invertebrate models to humans.Metabolic brain disease · 2026Review
- GluD1 at the synaptic crossroads: from domain structure to circuit dysfunction.Acta pharmacologica Sinica · 2026Review
- Glutamate delta-1 receptors regulate a tonic excitatory conductance in the mouse bed nucleus of the stria terminalis and influence neuronal function.Psychopharmacology · 2026Article
- Glutamate Delta 1 Receptor in Synapses, Circuits, and Disease.The European journal of neuroscience · 2026Review
- Deletion of Glutamate Delta 1 Receptor Leads to Heterogeneous Transcription and Synaptic Gene Alterations Across Brain Regions.International journal of molecular sciences · 2025Article
- Novel histone deacetylase-5 inhibitor T2943 exerts an anti-depressive effect in mice by enhancing GRID1 expression.Scientific reports · 2025Article
- Biological, genetic, neurological and environmental influences on homosexuality-a narrative review.Frontiers in behavioral neuroscience · 2025Review
- Ultrastructural Localization of Glutamate Delta Receptor 1 in the Rodent and Primate Lateral Habenula.The Journal of comparative neurology · 2025Article
- NMDA Receptors in Neurodevelopmental Disorders: Pathophysiology and Disease Models.International journal of molecular sciences · 2024Review
- Establishment of a Mitochondrial Metabolism-Related Diagnostic Model in Schizophrenia Based on LASSO Algorithm.Psychiatry investigation · 2024Article
- GRID1/GluD1 homozygous variants linked to intellectual disability and spastic paraplegia impair mGlu1/5 receptor signaling and excitatory synapses.Molecular psychiatry · 2024Article
- Clinical features, functional consequences, and rescue pharmacology of missense GRID1 and GRID2 human variants.Human molecular genetics · 2024Article
- Glutamate receptor genetic variants affected peripheral glutamatergic transmission and treatment induced improvement of Indian ADHD probands.Scientific reports · 2023Article
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Potentiation of neuronal activity by tonic GluD1 current in brain slices.EMBO reports · 2023Article
- The ortholog of human ssDNA-binding protein SSBP3 influences neurodevelopment and autism-like behaviors in Drosophila melanogaster.PLoS biology · 2023Article
- GluD receptors are functional ion channels.Biophysical journal · 2023Review
- LRFN5 and OLFM4 as novel potential biomarkers for major depressive disorder: a pilot study.Translational psychiatry · 2023Article
- Article
- A pharmacogenetic study of perampanel: association between rare variants of glutamate receptor genes and outcomes.Frontiers in genetics · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The delta family of ionotropic glutamate receptors consists of glutamate δ1 (GluD1) and glutamate δ2 (GluD2) receptors. While the role of GluD2 in the regulation of cerebellar physiology is well understood, the function of GluD1 in the central nervous system remains elusive. We demonstrate for the first time that deletion of GluD1 leads to abnormal emotional and social behaviors. We found that GluD1 knockout mice (GluD1 KO) were hyperactive, manifested lower anxiety-like behavior, depression-like behavior in a forced swim test and robust aggression in the resident-intruder test. Chronic lithium rescued the depression-like behavior in GluD1 KO. GluD1 KO mice also manifested deficits in social interaction. In the sociability test, GluD1 KO mice spent more time interacting with an inanimate object compared to a conspecific mouse. D-Cycloserine (DCS) administration was able to rescue social interaction deficits observed in GluD1 KO mice. At a molecular level synaptoneurosome preparations revealed lower GluA1 and GluA2 subunit expression in the prefrontal cortex and higher GluA1, GluK2 and PSD95 expression in the amygdala of GluD1 KO. Moreover, DCS normalized the lower GluA1 expression in prefrontal cortex of GluD1 KO. We propose that deletion of GluD1 leads to aberrant circuitry in prefrontal cortex and amygdala owing to its potential role in presynaptic differentiation and synapse formation. Furthermore, these findings are in agreement with the human genetic studies suggesting a strong association of GRID1 gene with several neuropsychiatric disorders including schizophrenia, bipolar disorder, autism spectrum disorders and major depressive disorder.
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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.