ReviewMolecular psychiatry2022
Relevance of interactions between dopamine and glutamate neurotransmission in schizophrenia.
Review in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Bioenergetic impairment in schizophrenia: role of mitochondrial signaling in synaptic dysfunction - a systematic review.Frontiers in cell and developmental biology · 2026Pooled it
- Glutamatergic Modulation of Brain Function in Psychosis: A Systematic Review of Neuroimaging Studies.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2025Pooled it
- Rational and Translational Implications of D-Amino Acids for Treatment-Resistant Schizophrenia: From Neurobiology to the Clinics.Biomolecules · 2022Pooled it
- Cognitive function differences across subtypes of first-episode antipsychotic-naïve schizophrenia: insights from event-related potentials.European archives of psychiatry and clinical neuroscience · 2026Article
- Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026Review
- Glucosamine/chitosan blend surface-engineered rutin-loaded polymer/lipid hybrid nanoparticles for neuroprotection in induced schizophrenia model.Scientific reports · 2026Article
- Single-cell transcriptomics revealed molecular vulnerability in a human midbrain-like organoid model of Parkinson's disease.iScience · 2026Article
- Artificial Intelligence Meets Ultra-High-Field Neuroimaging to Examine Psychosis.Biological psychiatry global open science · 2026Article
- Unraveling the mysteries of schizophrenia: Insights into prefrontal cortex dysfunction and therapeutic implications.World journal of psychiatry · 2025Review
- Measurement of Glutamate Suppression in a 6-OHDA-Induced Dopamine Deficiency Rat Model Following Acute Single-Dose L-DOPA Using GluCEST/MRS.Biomedicines · 2025Article
- Effectiveness of deep brain stimulation in alleviating treatment-resistant schizophrenia: a systematic review.European journal of translational myology · 2025Article
- Whole transcriptome sequencing to uncover CircRNA expression patterns linked to schizophrenia pathogenesis.European journal of medical research · 2025Article
- Association Between the (GT)26 Allele in the GRIN2A Promoter and Opioid Use Disorder.Psychiatry investigation · 2025Article
- Developing algorithmic psychiatry via multi-level spanning computational models.Cell reports. Medicine · 2025Review
- Mechanisms of Flame Retardant Toxicity and Their Impacts on Anxiety and Cognition in the Brain.Endocrinology · 2025Review
- Effect of Paliperidone Combined with Sertraline in the Treatment of Schizophrenia and its Influence on Serum Neurofunctional Related Factors.Alpha psychiatry · 2025Article
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Advancement in utilization of magnetic resonance imaging and biomarkers in the understanding of schizophrenia.World journal of clinical cases · 2025Article
- Nrf2 and Ferroptosis: Exploring Translational Avenues for Therapeutic Approaches to Neurological Diseases.Current drug targets · 2025Review
- Neuron-Derived Extracellular Vesicles miRNA Profiles Identify Children Who Experience Adverse Events after Ketamine Administration for Procedural Sedation.Clinical pharmacology and therapeutics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Dopamine (DA) and glutamate neurotransmission are strongly implicated in schizophrenia pathophysiology. While most studies focus on contributions of neurons that release only DA or glutamate, neither DA nor glutamate models alone recapitulate the full spectrum of schizophrenia pathophysiology. Similarly, therapeutic strategies limited to either system cannot effectively treat all three major symptom domains of schizophrenia: positive, negative, and cognitive symptoms. Increasing evidence suggests extensive interactions between the DA and glutamate systems and more effective treatments may therefore require the targeting of both DA and glutamate signaling. This offers the possibility that disrupting DA-glutamate circuitry between these two systems, particularly in the striatum and forebrain, culminate in schizophrenia pathophysiology. Yet, the mechanisms behind these interactions and their contributions to schizophrenia remain unclear. In addition to circuit- or system-level interactions between neurons that solely release either DA or glutamate, here we posit that functional alterations involving a subpopulation of neurons that co-release both DA and glutamate provide a novel point of integration between DA and glutamate systems, offering a key missing link in our understanding of schizophrenia pathophysiology. Better understanding of mechanisms underlying DA/glutamate co-release from these neurons may therefore shed new light on schizophrenia pathophysiology and lead to more effective therapeutics.
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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.