ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Motor neurons are selectively vulnerable to AMPA/kainate receptor-mediated injury in vitro.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it, 418 citations in OpenAlex.
- A standardized framework resolves ambiguity in motor neuron loss across neurodegenerative diseases.Acta neuropathologica communications · 2026Pooled it
- Randomized phase 2 study of perampanel for sporadic amyotrophic lateral sclerosis.Journal of neurology · 2022Trial
- A standardized framework resolves ambiguity in motor neuron loss across neurodegenerative diseases.bioRxiv : the preprint server for biology · 2026Article
- Multi-Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures.Journal of neurochemistry · 2025Article
- Myelin Lipid Alterations in Neurodegenerative Diseases: Landscape and Pathogenic Implications.Antioxidants & redox signaling · 2024Review
- Dynactin-1 mediates rescue of impaired axonal transport due to reduced mitochondrial bioenergetics in amyotrophic lateral sclerosis motor neurons.Brain communications · 2024Article
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- Impact of Plant-Derived Compounds on Amyotrophic Lateral Sclerosis.Neurotoxicity research · 2023Review
- ComparativeFrontiers in neuroscience · 2023Article
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- Structural basis of AMPA receptor inhibition by trans-4-butylcyclohexane carboxylic acid.British journal of pharmacology · 2022Article
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- Histopathological changes of the spinal cord and motor neuron dynamics in SOD1 Tg mice.Journal of toxicologic pathology · 2022Article
- NeuriTES. Monitoring neurite changes through transfer entropy and semantic segmentation in bright-field time-lapse microscopy.Patterns (New York, N.Y.) · 2021Article
- Bioengineered model of the human motor unit with physiologically functional neuromuscular junctions.Scientific reports · 2021Article
- A Human-Based Functional NMJ System for Personalized ALS Modeling and Drug Testing.Advanced therapeutics · 2020Article
- Prevention of mitochondrial impairment by inhibition of protein phosphatase 1 activity in amyotrophic lateral sclerosis.Cell death & disease · 2020Article
- Poly-arginine-18 (R18) Confers Neuroprotection through Glutamate Receptor Modulation, Intracellular Calcium Reduction, and Preservation of Mitochondrial Function.Molecules (Basel, Switzerland) · 2020Article
- Clinical and Molecular Aspects of Senataxin Mutations in Amyotrophic Lateral Sclerosis 4.Annals of neurology · 2020Article
- Acute Cellular and Functional Changes With a Combinatorial Treatment of Ion Channel Inhibitors Following Spinal Cord Injury.Frontiers in molecular neuroscience · 2020Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The nonphosphorylated neurofilament marker SMI-32 stains motor neurons in spinal cord slices and stains a subset of cultured spinal neurons ["large SMI-32(+) neurons"], which have a morphology consistent with motor neurons identified in vitro: large cell body, long axon, and extensive dendritic arborization. They are found preferentially in ventral spinal cord cultures, providing further evidence that large SMI-32(+) neurons are indeed motor neurons, and SMI-32 staining often colocalizes with established motor neuron markers (including acetylcholine, calcitonin gene-related peptide, and peripherin). Additionally, choline acetyltransferase activity (a frequently used index of the motor neuron population) and peripherin(+) neurons share with large SMI-32(+) neurons an unusual vulnerability to AMPA/kainate receptor-mediated injury. Kainate-induced loss of these motor neuron markers is Ca2+-dependent, which supports a critical role of Ca2+ ions in this injury. Raising extracellular Ca2+ exacerbates injury, whereas removal of extracellular Ca2+ is protective. A basis for this vulnerability is provided by the observation that most peripherin(+) neurons, like large SMI-32(+) neurons, are subject to kainate-stimulated Co2+ uptake, a histochemical stain that identifies neurons possessing Ca2+-permeable AMPA/kainate receptor-gated channels. Finally, of possibly greater relevance to the slow motor neuronal degeneration in diseases, both large SMI-32(+) neurons and peripherin(+) neurons are selectively damaged by prolonged (24 hr) low-level exposures to kainate (10 microM) or to the glutamate reuptake blocker L-trans-pyrrolidine-2,4-dicarboxylic acid (100 microM). During these low-level kainate exposures, large SMI-32(+) neurons showed higher intracellular Ca2+ concentrations than most spinal neurons, suggesting that Ca2+ ions are also important in this more slowly evolving injury.
Indexed as
Identifiers
8753869PMC6578994W1903414318What 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.