ArticleNeuron2013
Reversal of behavioral deficits and synaptic dysfunction in mice overexpressing neuregulin 1.
Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 90 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
90 citing papers in PubMed, 141 citations in OpenAlex.
- Drug Repurposing for Treating NCOR-Related Intellectual Disability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Antagonizing NRG1-ERBB4 signaling pathway with spironolactone for the treatment of schizophrenia: results of a randomized controlled drug repositioning clinical trial.Communications medicine · 2026Article
- Dynamic regulation of mRNA acetylation at synapses by spatial memory in mouse hippocampus.eLife · 2026Article
- Electroacupuncture attenuates anxiety caused by chronic mild stress through inhibiting NOX2-derived oxidative stress in ventral hippocampus.Neurobiology of stress · 2025Article
- Neddylation E1 Obligatory Subunit Nae1 Is Critical to Neuromuscular Junction Development and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Nrg1 intracellular signaling regulates the development of interhemispheric callosal axons in mice.Life science alliance · 2024Article
- nNOS in Erbb4-positive neurons regulates GABAergic transmission in mouse hippocampus.Cell death & disease · 2024Article
- HDAC9-mediated calmodulin deacetylation induces memory impairment in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- Article
- Integrative bioinformatics and artificial intelligence analyses of transcriptomics data identified genes associated with major depressive disorders includingNeurobiology of stress · 2023Article
- DiGeorge syndrome critical region gene 2 (DGCR2), a schizophrenia risk gene, regulates dendritic spine development through cell adhesion.Cell & bioscience · 2023Article
- Developmental loss of ErbB4 in PV interneurons disrupts state-dependent cortical circuit dynamics.Molecular psychiatry · 2023Article
- Genetic labeling reveals spatial and cellular expression pattern of neuregulin 1 in mouse brain.Cell & bioscience · 2023Article
- LIM Kinases, LIMK1 and LIMK2, Are Crucial Node Actors of the Cell Fate: Molecular to Pathological Features.Cells · 2023Review
- The laterodorsal tegmentum-ventral tegmental area circuit controls depression-like behaviors by activating ErbB4 in DA neurons.Molecular psychiatry · 2023Article
- NRG1 knockdown rescues PV interneuron GABAergic maturation deficits and schizophrenia behaviors in fetal growth restriction mice.Cell death discovery · 2022Article
- Investigating the Role of GABA in Neural Development and Disease Using Mice Lacking GAD67 or VGAT Genes.International journal of molecular sciences · 2022Review
- An alternative splicing hypothesis for neuropathology of schizophrenia: evidence from studies on historical candidate genes and multi-omics data.Molecular psychiatry · 2022Review
- Efficacy of Spironolactone as an Adjunctive Therapy to Risperidone to Improve Symptoms of Schizophrenia: A Double-Blind, Randomized, Placebo-Controlled, Clinical Trial.Iranian journal of psychiatry · 2022Article
- Steroid Receptor Coactivator 3 Regulates Synaptic Plasticity and Hippocampus-dependent Memory.Neuroscience bulletin · 2021Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Neuregulin 1 (Nrg1) is a susceptibility gene of schizophrenia, a disabling mental illness that affects 1% of the general population. Here, we show that ctoNrg1 mice, which mimic high levels of NRG1 observed in forebrain regions of schizophrenic patients, exhibit behavioral deficits and hypofunction of glutamatergic and GABAergic pathways. Intriguingly, these deficits were diminished when NRG1 expression returned to normal in adult mice, suggesting that damage which occurred during development is recoverable. Conversely, increase of NRG1 in adulthood was sufficient to cause glutamatergic impairment and behavioral deficits. We found that the glutamatergic impairment by NRG1 overexpression required LIM domain kinase 1 (LIMK1), which was activated in mutant mice, identifying a pathological mechanism. These observations demonstrate that synaptic dysfunction and behavioral deficits in ctoNrg1 mice require continuous NRG1 abnormality in adulthood, suggesting that relevant schizophrenia may benefit from therapeutic intervention to restore NRG1 signaling.
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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.