ArticleProceedings of the National Academy of Sciences of the United States of America2018
Genetic recovery of ErbB4 in adulthood partially restores brain functions in null mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
38 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- Restoration of Excitation-Inhibition Balance and Improvement of Schizophrenia-like Behavioral Deficits via Electroacupuncture.CNS neuroscience & therapeutics · 2026Article
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- Gonadotropin-releasing hormone alleviates chronic pain-related depression in male mice by rebalancing the anterior cingulate cortex excitatory-inhibitory processes via the protein kinase C/Erb-B2 receptor tyrosine kinase 4 pathway.Brain communications · 2026Article
- Exploration of schizophrenia-related behavioral and molecular abnormalities in a mutant mouse model with a mutation in the TVV motif of the ErbB4 gene.Molecular brain · 2025Article
- A systematic review on type 3 diabetes: bridging the gap between metabolic dysfunction and Alzheimer's disease.Diabetology & metabolic syndrome · 2025Review
- Common Genomic and Proteomic Alterations Related to Disturbed Neural Oscillatory Activity in Schizophrenia.International journal of molecular sciences · 2025Review
- MicroRNA-138-5p suppresses excitatory synaptic strength at the cerebellar input layer.The Journal of physiology · 2025Article
- ErbB4 deficiency exacerbates olfactory dysfunction in an early-stage Alzheimer's disease mouse model.Acta pharmacologica Sinica · 2024Article
- Review
- Parvalbumin interneuron deficits in schizophrenia.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2024Review
- nNOS in Erbb4-positive neurons regulates GABAergic transmission in mouse hippocampus.Cell death & disease · 2024Article
- Cellular Characterization and Interspecies Evolution of the Tree Shrew Retina across Postnatal Lifespan.Research (Washington, D.C.) · 2024Article
- Energy Expenditure Homeostasis Requires ErbB4, an Obesity Risk Gene, in the Paraventricular Nucleus.eNeuro · 2023Article
- Developmental loss of ErbB4 in PV interneurons disrupts state-dependent cortical circuit dynamics.Molecular psychiatry · 2023Article
- Dysregulation of ErbB4 Signaling Pathway in the Dorsal Hippocampus after Neonatal Hypoxia-Ischemia and Late Deficits in PVInternational journal of molecular sciences · 2022Article
- Toxic and Phenotypic Effects of AAV_Cre Used to Transduce Mesencephalic Dopaminergic Neurons.International journal of molecular sciences · 2022Article
- A novel spinal neuron connection for heat sensation.Neuron · 2022Article
- Developmental, neurochemical, and behavioral analyses of ErbB4 Cyt-1 knockout mice.Journal of neurochemistry · 2022Article
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurotrophic factor NRG1 and its receptor ErbB4 play a role in GABAergic circuit assembly during development. ErbB4 null mice possess fewer interneurons, have decreased GABA release, and show impaired behavior in various paradigms. In addition, NRG1 and ErbB4 have also been implicated in regulating GABAergic transmission and plasticity in matured brains. However, current ErbB4 mutant strains are unable to determine whether phenotypes in adult mutant mice result from abnormal neural development. This important question, a glaring gap in understanding NRG1-ErbB4 function, was addressed by using two strains of mice with temporal control of ErbB4 deletion and expression, respectively. We found that ErbB4 deletion in adult mice impaired behavior and GABA release but had no effect on neuron numbers and morphology. On the other hand, some deficits due to the ErbB4 null mutation during development were alleviated by restoring ErbB4 expression at the adult stage. Together, our results indicate a critical role of NRG1-ErbB4 signaling in GABAergic transmission and behavior in adulthood and suggest that restoring NRG1-ErbB4 signaling at the postdevelopmental stage might benefit relevant brain disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.