ArticleMolecular autism2016
Synaptic vesicle dynamic changes in a model of fragile X.
Article in Molecular autism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Proteomics insights into fragile X syndrome: Unraveling molecular mechanisms and therapeutic avenues.Neurobiology of disease · 2024Review
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Brain-specific deletion of GIT1 impairs cognition and alters phosphorylation of synaptic protein networks implicated in schizophrenia susceptibility.Molecular psychiatry · 2022Article
- Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective.Non-coding RNA · 2021Review
- FMRP Control of Ribosome Translocation Promotes Chromatin Modifications and Alternative Splicing of Neuronal Genes Linked to Autism.Cell reports · 2020Article
- Long-Term Plasticity of Neurotransmitter Release: Emerging Mechanisms and Contributions to Brain Function and Disease.Annual review of neuroscience · 2018Review
- Integrative bioinformatics analysis characterizing the role of EDC3 in mRNA decay and its association to intellectual disability.BMC medical genomics · 2018Article
- Impaired GABA Neural Circuits Are Critical for Fragile X Syndrome.Neural plasticity · 2018Review
- Parallel changes in serum proteins and diffusion tensor imaging in methamphetamine-associated psychosis.Scientific reports · 2017Article
- A brain proteomic investigation of rapamycin effects in theMolecular autism · 2017Article
- Screening the Molecular Framework Underlying Local Dendritic mRNA Translation.Frontiers in molecular neuroscience · 2017Review
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFragile X syndrome (FXS) is a single-gene disorder that is the most common heritable cause of intellectual disability and the most frequent monogenic cause of autism spectrum disorders (ASD). FXS is caused by an expansion of trinucleotide repeats in the promoter region of the fragile X mental retardation gene (Fmr1). This leads to a lack of fragile X mental retardation protein (FMRP), which regulates translation of a wide range of messenger RNAs (mRNAs). The extent of expression level alterations of synaptic proteins affected by FMRP loss and their consequences on synaptic dynamics in FXS has not been fully investigated.
methodsHere, we used an Fmr1 knockout (KO) mouse model to investigate the molecular mechanisms underlying FXS by monitoring protein expression changes using shotgun label-free liquid-chromatography mass spectrometry (LC-MS(E)) in brain tissue and synaptosome fractions. FXS-associated candidate proteins were validated using selected reaction monitoring (SRM) in synaptosome fractions for targeted protein quantification. Furthermore, functional alterations in synaptic release and dynamics were evaluated using live-cell imaging, and interpretation of synaptic dynamics differences was investigated using electron microscopy.
resultsKey findings relate to altered levels of proteins involved in GABA-signalling, especially in the cerebellum. Further exploration using microscopy studies found reduced synaptic vesicle unloading of hippocampal neurons and increased vesicle unloading in cerebellar neurons, which suggests a general decrease of synaptic transmission.
conclusionsOur findings suggest that FMRP is a regulator of synaptic vesicle dynamics, which supports the role of FMRP in presynaptic functions. Taken together, these studies provide novel insights into the molecular changes associated with FXS.
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