ArticleMolecular psychiatry2018
GluD1, linked to schizophrenia, controls the burst firing of dopamine neurons.
Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- GluD1 is localized at cholinergic synapses and is an acetylcholine receptor.Molecular psychiatry · 2026Article
- Inhibition of delta-1 glutamate receptor current by extracellular protons.bioRxiv : the preprint server for biology · 2026Article
- GluDs are ionotropic dopamine receptors tuned by G-proteins.bioRxiv : the preprint server for biology · 2026Article
- Molecular basis for ligand-gating of the human GluD1 receptor.bioRxiv : the preprint server for biology · 2026Article
- Urbanisation Drives Microevolution in the Egyptian Fruit Bat (Evolutionary applications · 2026Article
- GluD1 at the synaptic crossroads: from domain structure to circuit dysfunction.Acta pharmacologica Sinica · 2026Review
- A Cre-dependent lentiviral vector for neuron subtype-specific expression of large proteins.FEBS letters · 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
- Article
- D-Serine disrupts Cbln1 and GluD1 interaction and affects Cbln1-dependent synaptic effects and nocifensive responses in the central amygdala.Cellular and molecular life sciences : CMLS · 2025Article
- Ultrastructural Localization of Glutamate Delta Receptor 1 in the Rodent and Primate Lateral Habenula.The Journal of comparative neurology · 2025Article
- Dopamine builds and reveals reward-associated latent behavioral attractors.Nature communications · 2024Article
- Identification of novel genetic loci related to dromedary camel (Camelus dromedarius) morphometrics, biomechanics, and behavior by genome-wide association studies.BMC veterinary research · 2024Article
- Lack of evidence for direct ligand-gated ion channel activity of GluD receptors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Metabotropic signaling within somatostatin interneurons controls transient thalamocortical inputs during development.Nature communications · 2024Article
- Two Signaling Modes Are Better than One: Flux-Independent Signaling by Ionotropic Glutamate Receptors Is Coming of Age.Biomedicines · 2024Review
- GRID1/GluD1 homozygous variants linked to intellectual disability and spastic paraplegia impair mGlu1/5 receptor signaling and excitatory synapses.Molecular psychiatry · 2024Article
- Loss of activation by GABA in vertebrate delta ionotropic glutamate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Potentiation of neuronal activity by tonic GluD1 current in brain slices.EMBO reports · 2023Article
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human mutations of the GRID1 gene encoding the orphan delta1 glutamate receptor-channel (GluD1) are associated with schizophrenia but the explicit role of GluD1 in brain circuits is unknown. Based on the known function of its paralog GluD2 in cerebellum, we searched for a role of GluD1 in slow glutamatergic transmission mediated by metabotropic receptor mGlu1 in midbrain dopamine neurons, whose dysfunction is a hallmark of schizophrenia. We found that an mGlu1 agonist elicits a slow depolarizing current in HEK cells co-expressing mGlu1 and GluD1, but not in cells expressing mGlu1 or GluD1 alone. This current is abolished by additional co-expression of a dominant-negative GluD1 dead pore mutant. We then characterized mGlu1-dependent currents in dopamine neurons from midbrain slices. Both the agonist-evoked and the slow postsynaptic currents are abolished by expression of the dominant-negative GluD1 mutant, pointing to the involvement of native GluD1 channels in these currents. Likewise, both mGlu1-dependent currents are suppressed in GRID1 knockout mice, which reportedly display endophenotypes relevant for schizophrenia. It is known that mGlu1 activation triggers the transition from tonic to burst firing of dopamine neurons, which signals salient stimuli and encodes reward prediction. In vivo recordings of dopamine neurons showed that their spontaneous burst firing is abolished in GRID1 knockout mice or upon targeted expression of the dominant-negative GluD1 mutant in wild-type mice. Our results de-orphanize GluD1, unravel its key role in slow glutamatergic transmission and provide insights into how GRID1 gene alterations can lead to dopaminergic dysfunctions in schizophrenia.
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