ArticlePLoS biology2021
Synaptotagmin-7-mediated activation of spontaneous NMDAR currents is disrupted in bipolar disorder susceptibility variants.
Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- IL-1β pathway-dependent regulation of glutamate receptor activity by gut microbiota in bipolar depression.Journal of Zhejiang University. Science. B · 2026Article
- 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
- Silibinin's role in counteracting neuronal apoptosis and synaptic dysfunction in Alzheimer's disease models.Apoptosis : an international journal on programmed cell death · 2025Article
- Pathological Interplay between Inflammation and Mitochondria Aggravates Glutamate Toxicity.International journal of molecular sciences · 2024Review
- 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
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Synaptotagmin-7 (Syt7) plays direct or redundant Ca2+ sensor roles in multiple forms of vesicle exocytosis in synapses. Here, we show that Syt7 is a redundant Ca2+ sensor with Syt1/Doc2 to drive spontaneous glutamate release, which functions uniquely to activate the postsynaptic GluN2B-containing NMDARs that significantly contribute to mental illness. In mouse hippocampal neurons lacking Syt1/Doc2, Syt7 inactivation largely diminishes spontaneous release. Using 2 approaches, including measuring Ca2+ dose response and substituting extracellular Ca2+ with Sr2+, we detect that Syt7 directly triggers spontaneous release via its Ca2+ binding motif to activate GluN2B-NMDARs. Furthermore, modifying the localization of Syt7 in the active zone still allows Syt7 to drive spontaneous release, but the GluN2B-NMDAR activity is abolished. Finally, Syt7 SNPs identified in bipolar disorder patients destroy the function of Syt7 in spontaneous release in patient iPSC-derived and mouse hippocampal neurons. Therefore, Syt7 could contribute to neuropsychiatric disorders through driving spontaneous glutamate release.
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