ArticleNeuroscience2009
Alterations in corticostriatal synaptic plasticity in mice overexpressing human alpha-synuclein.
Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
- Impairment in stimulus-response learning as a cognitive biomarker in a model of synucleinopathy.Translational psychiatry · 2026Article
- Alpha-synuclein overexpression reduces neural activity within a basal ganglia vocal nucleus in a zebra finch model.PloS one · 2026Article
- Glutamatergic synaptic resilience to overexpressed human alpha-synuclein.NPJ Parkinson's disease · 2025Article
- Adenosine AInternational journal of molecular sciences · 2024Article
- Alpha synuclein post translational modifications: potential targets for Parkinson's disease therapy?Frontiers in molecular neuroscience · 2023Review
- The Role of Membrane Affinity and Binding Modes in Alpha-Synuclein Regulation of Vesicle Release and Trafficking.Biomolecules · 2022Article
- C-terminal truncation modulates α-Synuclein's cytotoxicity and aggregation by promoting the interactions with membrane and chaperone.Communications biology · 2022Article
- Aromaticity at position 39 in α-synuclein: A modulator of amyloid fibril assembly and membrane-bound conformations.Protein science : a publication of the Protein Society · 2022Article
- Alpha-Synuclein is Involved in DYT1 Dystonia Striatal Synaptic Dysfunction.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Up and Down γ-Synuclein Transcription in Dopamine Neurons Translates into Changes in Dopamine Neurotransmission and Behavioral Performance in Mice.International journal of molecular sciences · 2022Article
- Linking α-synuclein-induced synaptopathy and neural network dysfunction in early Parkinson's disease.Brain communications · 2022Review
- Brain regions susceptible to alpha-synuclein spreading.Molecular psychiatry · 2022Review
- α-Synuclein kinetically regulates the nascent fusion pore dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Genes Implicated in Familial Parkinson's Disease Provide a Dual Picture of Nigral Dopaminergic Neurodegeneration with Mitochondria Taking Center Stage.International journal of molecular sciences · 2021Review
- Differential Regional Responses in Soluble Monomeric Alpha Synuclein Abundance Following Traumatic Brain Injury.Molecular neurobiology · 2021Article
- Molecular Mechanisms of Glutamate Toxicity in Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Enhanced mitochondrial inhibition by 3,4-dihydroxyphenyl-acetaldehyde (DOPAL)-oligomerized α-synuclein.Journal of neuroscience research · 2019Article
- Membrane interactions of intrinsically disordered proteins: The example of alpha-synuclein.Biochimica et biophysica acta. Proteins and proteomics · 2019Review
- Inflammation, Infectious Triggers, and Parkinson's Disease.Frontiers in neurology · 2019Review
- Chronic nicotine improves cognitive and social impairment in mice overexpressing wild type α-synuclein.Neurobiology of disease · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Most forms of Parkinson's disease (PD) are sporadic in nature, but some have genetic causes as first described for the alpha-synuclein gene. The alpha-synuclein protein also accumulates as insoluble aggregates in Lewy bodies in sporadic PD as well as in most inherited forms of PD. The focus of the present study is the modulation of synaptic plasticity in the corticostriatal pathway of transgenic (Tg) mice that overexpress the human alpha-synuclein protein throughout the brain (ASOTg). Paired-pulse facilitation was detected in vitro by activation of corticostriatal afferents in ASOTg mice, consistent with a presynaptic effect of elevated human alpha-synuclein. However basal synaptic transmission was unchanged in ASOTg, suggesting that human alpha-synuclein could impact paired-pulse facilitation via a presynaptic mechanism not directly related to the probability of neurotransmitter release. Mice lacking alpha-synuclein or those expressing normal and A53T human alpha-synuclein in tyrosine hydroxylase-containing neurons showed, instead, paired-pulse depression. High-frequency stimulation induced a presynaptic form of long-term depression solely in ASOTg striatum. A presynaptic, N-methyl-d-aspartate receptor-independent form of chemical long-term potentiation induced by forskolin (FSK) was enhanced in ASOTg striatum, while FSK-induced cAMP levels were reduced in ASOTg synaptoneurosome fractions. Overall the results suggest that elevated human alpha-synuclein alters presynaptic plasticity in the corticostriatal pathway, possibly reflecting a reduction in glutamate at corticostriatal synapses by modulation of adenylyl cyclase signaling pathways. ASOTg mice may recapitulate an early stage in PD during which overexpressed alpha-synuclein dampens corticostriatal synaptic transmission and reduces movement.
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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.