ArticleBrain and behavior2023
In vivo overexpression of synaptogyrin-3 promotes striatal synaptic dopamine uptake in LRRK2
Article in Brain and behavior, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 15 citations in OpenAlex.
- A machine learning approach to identify key epigenetic transcripts for ageing research in human blood (Epitage).Biogerontology · 2026Article
- Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson's Disease.Biomedicines · 2026Review
- Role of LRRK2 in physiological activities, diseases, and therapy.Chinese medical journal · 2026Review
- Synaptogyrin-3 plays a critical role in addiction-related dopamine dysfunction and behavioral maladaptations.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.eLife · 2025Article
- Affective phenotypes in heterozygousFrontiers in genetics · 2025Article
- Integrative analysis of plasma and substantia nigra in Parkinson's disease: unraveling biomarkers and insights from the lncRNA-miRNA-mRNA ceRNA network.Frontiers in aging neuroscience · 2024Article
- Molecular Mechanisms Underlying Chronic and Degenerative Diseases.International journal of molecular sciences · 2023Article
- In vivo overexpression of synaptogyrin-3 promotes striatal synaptic dopamine uptake in LRRK2Brain and behavior · 2023Article
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11 authors at 2 institutions in 2 countries.
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Abstract
backgroundLeucine-rich repeat kinase 2 (LRRK2) mutation is a common genetic risk factor of Parkinson's disease (PD). Presynaptic dysfunction is an early pathogenic event associated with dopamine (DA) dysregulation in striatum of the brain. DA uptake activity of DA uptake transporter (DAT) affects synaptic plasticity and motor and non-motor behavior. Synaptogyrin-3 (SYNGR3) is part of the synaptogyrin family, especially abundant in brain. Previous in vitro studies demonstrated interaction between SYNGR3 and DAT. Reduced SYNGR3 expression was observed in human PD brains with unclear reasons.
methodsHere, we further explored whether inducing SYNGR3 expression can influence (i) cellular DA uptake using differentiated human SH-SY5Y neuronal cells, (ii) striatal synaptosomal DA uptake in a mutant LRRK2
resultsYoung LRRK2 mutant mice exhibited significantly lower SYNGR3 levels in striatum compared to age-matched wild-type (WT) controls, resembling level in aged WT mice. SYNGR3 is spatially co-localized with DAT at striatal presynaptic terminals, visualized by immuno-gold transmission electron microscopy and immunohistochemistry. Their protein-protein interaction was confirmed by co-immunoprecipitation. Transient overexpression of SYNGR3 in differentiated SH-SY5Y cells increased cellular DA uptake activity without affecting total DAT levels. Inducing SYNGR3 overexpression by adeno-associated virus-7 (AAV7) injection in vivo into striatum increased ex vivo synaptosomal DA uptake in LRRK2 mutant mice and improved their innate marble burying behavior.
conclusionBrain SYNGR3 expression may be an important determinant to striatal DA homeostasis and synaptic function. Our preliminary behavioral test showed improved innate behavior after SYNGR3 overexpression in LRRK2 mutant mice, advocating further studies to determine the influence of SYNGR3 in the pathophysiology of DA neurons in PD.
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