ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Glutamate and amyloid beta-protein rapidly inhibit fast axonal transport in cultured rat hippocampal neurons by different mechanisms.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 106 citations in OpenAlex.
- Molecular Motors in Myelination and Their Misregulation in Disease.Molecular neurobiology · 2025Review
- Role of Cytoskeletal Elements in Regulation of Synaptic Functions: Implications Toward Alzheimer's Disease and Phytochemicals-Based Interventions.Molecular neurobiology · 2024Review
- Increases in anterograde axoplasmic transport in neurons of the hyper-glutamatergic, glutamate dehydrogenase 1 (Glud1) transgenic mouse: Effects of glutamate receptors on transport.Journal of neurochemistry · 2024Article
- Pathophysiology of neurodegenerative diseases: An interplay among axonal transport failure, oxidative stress, and inflammation?Seminars in immunology · 2022Review
- Sublingual AKBA Exerts Antidepressant Effects in the Aβ-Treated Mouse Model.Biomolecules · 2021Article
- Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.Biology open · 2021Review
- Acute Effects of Two Different Species of Amyloid-Neural plasticity · 2020Article
- Amyloid Plaques of Alzheimer's Disease as Hotspots of Glutamatergic Activity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Region-specific depletion of synaptic mitochondria in the brains of patients with Alzheimer's disease.Acta neuropathologica · 2018Article
- Interaction between a MAPT variant causing frontotemporal dementia and mutant APP affects axonal transport.Neurobiology of aging · 2018Article
- Upregulation of Vesicular Glutamate Transporter 2 and STAT3 Activation in the Spinal Cord of Mice Receiving 3,3'-Iminodipropionitrile.Neurotoxicity research · 2018Article
- Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer's disease -conformist, nonconformist, and realistic prospects for AD pathogenesis.Translational neurodegeneration · 2018Review
- The Physiological and Pathological Implications of the Formation of Hydrogels, with a Specific Focus on Amyloid Polypeptides.Biomolecules · 2017Review
- Axonal transport deficits in multiple sclerosis: spiraling into the abyss.Acta neuropathologica · 2017Review
- Article
- Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1.Acta neuropathologica · 2016Article
- Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Molecular neurobiology · 2015Review
- Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β.The Journal of cell biology · 2015Article
- Altered expression of neurofilament 200 and amyloid-β peptide (1-40) in a rat model of chronic cerebral hypoperfusion.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015Article
- Alzheimer's disease-related amyloid-β induces synaptotoxicity in human iPS cell-derived neurons.Cell death & disease · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impairment of axonal transport leads to neurodegeneration and synapse loss. Glutamate and amyloid beta-protein (Abeta) have critical roles in the pathogenesis of Alzheimer's disease (AD). Here we show that both agents rapidly inhibit fast axonal transport in cultured rat hippocampal neurons. The effect of glutamate (100 microm), but not of Abeta25-35 (20 microm), was reversible, was mimicked by NMDA or AMPA, and was blocked by NMDA and AMPA antagonists and by removal of extracellular Ca2+. The effect of Abeta25-35 was progressive and irreversible, was prevented by the actin-depolymerizing agent latrunculin B, and was mimicked by the actin-polymerizing agent jasplakinolide. Abeta25-35 induced intracellular actin aggregation, which was prevented by latrunculin B. Abeta31-35 but not Abeta15-20 exerted effects similar to those of Abeta25-35. Full-length Abeta1-42 incubated for 7 d, which specifically contained 30-100 kDa molecular weight assemblies, also caused an inhibition of axonal transport associated with intracellular actin aggregation, whereas freshly dissolved Abeta1-40, incubated Abeta1-40, and fresh Abeta1-42 had no effect. These results suggest that glutamate inhibits axonal transport via activation of NMDA and AMPA receptors and Ca2+ influx, whereas Abeta exerts its inhibitory effect via actin polymerization and aggregation. The ability of Abeta to inhibit axonal transport seems to require active amino acid residues, which is probably present in the 31-35 sequence. Full-length Abeta may be effective when it represents a structure in which these active residues can access the cell membrane. Our results may provide insight into the early pathogenetic mechanisms of AD.
Indexed as
Identifiers
14523099PMC6740390W1812263681What OpenQuestion holds
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.