ArticleNature neuroscience2017
Reduced sensory synaptic excitation impairs motor neuron function via Kv2.1 in spinal muscular atrophy.
Article in Nature neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- A standardized framework resolves ambiguity in motor neuron loss across neurodegenerative diseases.Acta neuropathologica communications · 2026Pooled it
- First-in-human study of epidural spinal cord stimulation in individuals with spinal muscular atrophy.Nature medicine · 2025Trial
- C3 and CD47 mediate sensory-motor circuit refinement during spinal cord development.The Journal of experimental medicine · 2026Article
- Cellular and molecular mechanisms of muscle spindle development and function.Physiology (Bethesda, Md.) · 2026Review
- Ten years of disease-modifying therapy in spinal muscular atrophy: lessons learned and future directions.Nature reviews. Neurology · 2026Review
- Incomplete cerebellar circuit restoration limits functional recovery following SMN therapy in severe spinal muscular atrophy.bioRxiv : the preprint server for biology · 2026Article
- Disease-Modifying Therapies in Spinal Muscular Atrophy: Neurodevelopmental and Behavioral Outcomes in the Treatment Era.Advances in therapy · 2026Review
- A p53-ΔNp73 signaling axis drives selective motor neuron degeneration in spinal muscular atrophy.bioRxiv : the preprint server for biology · 2026Article
- Long-term comparative analysis of AAV9-mediated gene replacement therapies for spinal muscular atrophy in mice.Nature communications · 2026Article
- Nanotube-Assisted Motor Neuron and Neuromuscular Junction Stabilization in Spinal Muscular Atrophy: A Hypothesis for Adjunctive Therapy.Neurology international · 2026Review
- A standardized framework resolves ambiguity in motor neuron loss across neurodegenerative diseases.bioRxiv : the preprint server for biology · 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
- Cerebellar pathology contributes to neurodevelopmental deficits in spinal muscular atrophy.Brain : a journal of neurology · 2026Article
- Nusinersen rescues taurine deficiency in patients with type 1 Spinal Muscular Atrophy.Communications medicine · 2026Article
- Immaturity of the neuromuscular junction in spinal muscular atrophy mouse models.Frontiers in cellular neuroscience · 2026Review
- Synaptopathy in the TDP-43ΔNLS Mouse Model of Sporadic Amyotrophic Lateral Sclerosis.The European journal of neuroscience · 2025Article
- Cerebellar defects are a primary pathology in mouse models of spinal muscular atrophy.Brain pathology (Zurich, Switzerland) · 2025Article
- Genetic Variants inInternational journal of molecular sciences · 2025Article
- Identification of p38 MAPK inhibition as a neuroprotective strategy for combinatorial SMA therapy.EMBO molecular medicine · 2025Article
- Nusinersen corrects L-arginine deficiency in the cerebrospinal fluid of patients with severe spinal muscular atrophy.Neurobiology of disease · 2025Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Behavioral deficits in neurodegenerative diseases are often attributed to the selective dysfunction of vulnerable neurons via cell-autonomous mechanisms. Although vulnerable neurons are embedded in neuronal circuits, the contributions of their synaptic partners to disease process are largely unknown. Here we show that, in a mouse model of spinal muscular atrophy (SMA), a reduction in proprioceptive synaptic drive leads to motor neuron dysfunction and motor behavior impairments. In SMA mice or after the blockade of proprioceptive synaptic transmission, we observed a decrease in the motor neuron firing that could be explained by the reduction in the expression of the potassium channel Kv2.1 at the surface of motor neurons. Chronically increasing neuronal activity pharmacologically in vivo led to a normalization of Kv2.1 expression and an improvement in motor function. Our results demonstrate a key role of excitatory synaptic drive in shaping the function of motor neurons during development and the contribution of its disruption to a neurodegenerative disease.
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What 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.