ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Defects in Motoneuron-Astrocyte Interactions in Spinal Muscular Atrophy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Haloperidol induces neuroprotection and enhances neuromuscular function in both murine and human models of spinal muscular atrophy.Experimental & molecular medicine · 2026Article
- Astrocyte targeted SMN1 gene therapy and forskolin application improves astrocyte filopodia actin defects and motor neuron synaptic dysfunction in human SMA disease pathology.bioRxiv : the preprint server for biology · 2026Article
- Unbiased bioinformatic and clinical analysis identifies glial fibrillary acidic protein as a potential biomarker in spinal muscular atrophy.Brain communications · 2026Article
- Comorbidities in spinal muscular atrophy and their impact on the course of the underlying disease: a real-life observational study.BMC musculoskeletal disorders · 2025Observational
- Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications.Neurology international · 2025Review
- PRMT inhibitor promotes SMN2 exon 7 inclusion and synergizes with nusinersen to rescue SMA mice.EMBO molecular medicine · 2023Article
- Antibody-oligonucleotide conjugate achieves CNS delivery in animal models for spinal muscular atrophy.JCI insight · 2022Article
- Microvasculopathy in spinal muscular atrophy is driven by a reversible autonomous endothelial cell defect.The Journal of clinical investigation · 2022Article
- Single-cell RNA sequencing reveals dysregulation of spinal cord cell types in a severe spinal muscular atrophy mouse model.PLoS genetics · 2022Article
- Glial fibrillary acidic protein in cerebrospinal fluid of patients with spinal muscular atrophy.Annals of clinical and translational neurology · 2022Article
- Moxifloxacin rescues SMA phenotypes in patient-derived cells and animal model.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Biological networks and complexity in early-onset motor neuron diseases.Frontiers in neurology · 2022Article
- Human sensorimotor organoids derived from healthy and amyotrophic lateral sclerosis stem cells form neuromuscular junctions.Nature communications · 2021Article
- Cell adhesion molecules regulating astrocyte-neuron interactions.Current opinion in neurobiology · 2021Review
- Metabolic Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2021Review
- SNAP25 Inhibits Glioma Progression by Regulating Synapse PlasticityFrontiers in oncology · 2021Article
- Drug Screening and Drug Repositioning as Promising Therapeutic Approaches for Spinal Muscular Atrophy Treatment.Frontiers in pharmacology · 2020Review
- Notch Signaling Mediates Astrocyte Abnormality in Spinal Muscular Atrophy Model Systems.Scientific reports · 2019Article
- Advances in therapy for spinal muscular atrophy: promises and challenges.Nature reviews. Neurology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal muscular atrophy (SMA) is a motoneuron disease caused by loss or mutation in Survival of Motor Neuron 1 (SMN1) gene. Recent studies have shown that selective restoration of SMN protein in astrocytes partially alleviates pathology in an SMA mouse model, suggesting important roles for astrocytes in SMA. Addressing these underlying mechanisms may provide new therapeutic avenues to fight SMA. Using primary cultures of pure motoneurons or astrocytes from SMNΔ7 (SMA) and wild-type (WT) mice, as well as their mixed and matched cocultures, we characterized the contributions of motoneurons, astrocytes, and their interactions to synapse loss in SMA. In pure motoneuron cultures, SMA motoneurons exhibited normal survival but intrinsic defects in synapse formation and synaptic transmission. In pure astrocyte cultures, SMA astrocytes exhibited defects in calcium homeostasis. In motoneuron-astrocyte contact cocultures, synapse formation and synaptic transmission were significantly reduced when either motoneurons, astrocytes or both were from SMA mice compared with those in WT motoneurons cocultured with WT astrocytes. The reduced synaptic activity is unlikely due to changes in motoneuron excitability. This disruption in synapse formation and synaptic transmission by SMN deficiency was not detected in motoneuron-astrocyte noncontact cocultures. Additionally, we observed a downregulation of Ephrin B2 in SMA astrocytes. These findings suggest that there are both cell autonomous and non-cell-autonomous defects in SMA motoneurons and astrocytes. Defects in contact interactions between SMA motoneurons and astrocytes impair synaptogenesis seen in SMA pathology, possibly due to the disruption of the Ephrin B2 pathway.
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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.