ArticleProceedings of the National Academy of Sciences of the United States of America2020
Synaptotagmin-7 is a key factor for bipolar-like behavioral abnormalities in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- Enhanced axonal mitochondrial motility and neural activity-induced energy deficits destabilize synaptic transmission in models of bipolar disorder.Nature communications · 2026Article
- Increased CA3 burst activity inbioRxiv : the preprint server for biology · 2026Article
- IL-1β pathway-dependent regulation of glutamate receptor activity by gut microbiota in bipolar depression.Journal of Zhejiang University. Science. B · 2026Article
- A pancreas-hippocampus feedback mechanism regulates circadian changes in depression-related behaviors.Nature neuroscience · 2025Article
- Microglia contribute to bipolar depression through Serinc2-dependent phospholipid synthesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bidirectional causal associations between plasma metabolites and bipolar disorder.Molecular psychiatry · 2025Article
- Human mood disorder risk gene Synaptotagmin-14 contributes to mania-like behaviors in mice.Molecular psychiatry · 2025Article
- Synaptotagmin-7 deficit causes insulin hypoactivity and contributes to behavioral alterations in mice.iScience · 2025Article
- NEK4 modulates circadian fluctuations of emotional behaviors and synaptogenesis in male mice.Nature communications · 2024Article
- Progress and Implications from Genetic Studies of Bipolar Disorder.Neuroscience bulletin · 2024Review
- Region-Related Differences in Short-Term Synaptic Plasticity and Synaptotagmin-7 in the Male and Female Hippocampus of a Rat Model of Fragile X Syndrome.International journal of molecular sciences · 2024Article
- Identification of Candidate Genes and Pathways Linked to the Temperament Trait in Sheep.Genes · 2024Article
- A single base pair substitution in zebrafish distinguishes between innate and acute startle behavior regulation.PloS one · 2024Article
- Dysfunction of cAMP-Protein Kinase A-Calcium Signaling Axis in Striatal Medium Spiny Neurons: A Role in Schizophrenia and Huntington's Disease Neuropathology.Biological psychiatry global open science · 2023Article
- Vesicle trafficking and vesicle fusion: mechanisms, biological functions, and their implications for potential disease therapy.Molecular biomedicine · 2022Review
- Phenotypes, mechanisms and therapeutics: insights from bipolar disorder GWAS findings.Molecular psychiatry · 2022Review
- Synaptotagmins 1 and 7 Play Complementary Roles in Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Gene expression in the amygdala and hippocampus of cyclic and acyclic gilts.Journal of animal science · 2022Article
- Article
- Synaptotagmin-7-mediated activation of spontaneous NMDAR currents is disrupted in bipolar disorder susceptibility variants.PLoS biology · 2021Article
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Authors and funding
22 authors at 10 institutions in 3 countries.
Funding
Abstract
The pathogenesis of bipolar disorder (BD) has remained enigmatic, largely because genetic animal models based on identified susceptible genes have often failed to show core symptoms of spontaneous mood cycling. However, pedigree and induced pluripotent stem cell (iPSC)-based analyses have implicated that dysfunction in some key signaling cascades might be crucial for the disease pathogenesis in a subpopulation of BD patients. We hypothesized that the behavioral abnormalities of patients and the comorbid metabolic abnormalities might share some identical molecular mechanism. Hence, we investigated the expression of insulin/synapse dually functioning genes in neurons derived from the iPSCs of BD patients and the behavioral phenotype of mice with these genes silenced in the hippocampus. By these means, we identified synaptotagmin-7 (Syt7) as a candidate risk factor for behavioral abnormalities. We then investigated Syt7 knockout (KO) mice and observed nocturnal manic-like and diurnal depressive-like behavioral fluctuations in a majority of these animals, analogous to the mood cycling symptoms of BD. We treated the Syt7 KO mice with clinical BD drugs including olanzapine and lithium, and found that the drug treatments could efficiently regulate the behavioral abnormalities of the Syt7 KO mice. To further verify whether Syt7 deficits existed in BD patients, we investigated the plasma samples of 20 BD patients and found that the Syt7 mRNA level was significantly attenuated in the patient plasma compared to the healthy controls. We therefore concluded that Syt7 is likely a key factor for the bipolar-like behavioral abnormalities.
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