ReviewMolecular neurobiology2011
NO orchestrates the loss of synaptic boutons from adult "sick" motoneurons: modeling a molecular mechanism.
Review in Molecular neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases.Journal of personalized medicine · 2026Review
- Value of synaptic proteins as biomarkers in amyotrophic lateral sclerosis.Brain communications · 2026Article
- Nitric oxide mediates activity-dependent change to synaptic excitation during a critical period in Drosophila.Scientific reports · 2021Article
- Article
- Lysophosphatidic Acid and Several Neurotransmitters Converge on Rho-Kinase 2 Signaling to Manage Motoneuron Excitability.Frontiers in molecular neuroscience · 2021Article
- Nitric oxide controls excitatory/inhibitory balance in the hypoglossal nucleus during early postnatal development.Brain structure & function · 2020Article
- Nitrosative Stress in the Frontal Cortex From Dogs With Canine Cognitive Dysfunction.Frontiers in veterinary science · 2020Article
- Synaptic Plasticity on Motoneurons After Axotomy: A Necessary Change in Paradigm.Frontiers in molecular neuroscience · 2020Review
- Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.Nature communications · 2019Article
- The Y172 Monoclonal Antibody Against p-c-Jun (Ser63) Is a Marker of the Postsynaptic Compartment of C-Type Cholinergic Afferent Synapses on Motoneurons.Frontiers in cellular neuroscience · 2019Article
- Article
- Membrane-derived phospholipids control synaptic neurotransmission and plasticity.PLoS biology · 2015Article
- S-nitrosation and neuronal plasticity.British journal of pharmacology · 2015Review
- Glycoursodeoxycholic acid reduces matrix metalloproteinase-9 and caspase-9 activation in a cellular model of superoxide dismutase-1 neurodegeneration.Molecular neurobiology · 2015Article
- Neuronal BDNF signaling is necessary for the effects of treadmill exercise on synaptic stripping of axotomized motoneurons.Neural plasticity · 2015Article
- Article
- Microglia centered pathogenesis in ALS: insights in cell interconnectivity.Frontiers in cellular neuroscience · 2014Review
- Nitric oxide synthesis and cGMP production is important for neurite growth and synapse remodeling after axotomy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Early presymptomatic cholinergic dysfunction in a murine model of amyotrophic lateral sclerosis.Brain and behavior · 2013Article
- Nitric oxide-mediated oxidative damage and the progressive demise of motor neurons in ALS.Neurotoxicity research · 2012Review
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
Synapse elimination is the main factor responsible for the cognitive decline accompanying many of the neuropathological conditions affecting humans. Synaptic stripping of motoneurons is also a common hallmark of several motor pathologies. Therefore, knowledge of the molecular basis underlying this plastic process is of central interest for the development of new therapeutic tools. Recent advances from our group highlight the role of nitric oxide (NO) as a key molecule triggering synapse loss in two models of motor pathologies. De novo expression of the neuronal isoform of NO synthase (nNOS) in motoneurons commonly occurs in response to the physical injury of a motor nerve and in the course of amyotrophic lateral sclerosis. In both conditions, this event precedes synaptic withdrawal from motoneurons. Strikingly, nNOS-synthesized NO is "necessary" and "sufficient" to induce synaptic detachment from motoneurons. The mechanism involves a paracrine/retrograde action of NO on pre-synaptic structures, initiating a downstream signaling cascade that includes sequential activation of (1) soluble guanylyl cyclase, (2) cyclic guanosine monophosphate-dependent protein kinase, and (3) RhoA/Rho kinase (ROCK) signaling. Finally, ROCK activation promotes phosphorylation of regulatory myosin light chain, which leads to myosin activation and actomyosin contraction. This latter event presumably contributes to the contractile force to produce ending axon retraction. Several findings support that this mechanism may operate in the most prevalent neurodegenerative diseases.
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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.