ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Calcium signaling pathways mediating synaptic potentiation triggered by amyotrophic lateral sclerosis IgG in motor nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed.
- Presynaptic compensation sustains neuromuscular transmission in the mouse diaphragm at a late stage of aging.Biogerontology · 2026Article
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
- Exogenous nanomolar zinc ion (ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Mechanisms of Cadmium Neurotoxicity.International journal of molecular sciences · 2023Review
- Immunology of amyotrophic lateral sclerosis - role of the innate and adaptive immunity.Frontiers in neuroscience · 2023Review
- L-type CaCellular and molecular neurobiology · 2022Article
- Modulation of spontaneous motor unit potentials by a new motor cortical magnetic stimulation method in amyotrophic lateral sclerosis.Journal of neurology · 2022Article
- Synaptic mechanisms of cadmium neurotoxicity.Neural regeneration research · 2021Article
- Selective Neuronal Death in Neurodegenerative Diseases: The Ongoing Mystery.The Yale journal of biology and medicine · 2019Review
- Pathophysiology and Diagnosis of ALS: Insights from Advances in Neurophysiological Techniques.International journal of molecular sciences · 2019Review
- The C9orf72-interacting protein Smcr8 is a negative regulator of autoimmunity and lysosomal exocytosis.Genes & development · 2018Article
- Immunoglobulins G from Sera of Amyotrophic Lateral Sclerosis Patients Induce Oxidative Stress and Upregulation of Antioxidative System in BV-2 Microglial Cell Line.Frontiers in immunology · 2017Article
- Complement activation at the motor end-plates in amyotrophic lateral sclerosis.Journal of neuroinflammation · 2016Article
- Immunoablation and Stem Cell Transplantation in Amyotrophic Lateral Sclerosis: The Ultimate Test for the Autoimmune Pathogenesis Hypothesis.Frontiers in neurology · 2016Review
- Novel molecular biomarkers at the blood-brain barrier in ALS.BioMed research international · 2014Review
- Neuroimmunity dynamics and the development of therapeutic strategies for amyotrophic lateral sclerosis.Frontiers in cellular neuroscience · 2013Review
- Transcranial magnetic stimulation and amyotrophic lateral sclerosis: pathophysiological insights.Journal of neurology, neurosurgery, and psychiatry · 2013Review
- Humoral immune activation in amyotrophic lateral sclerosis patients.Neurology international · 2013Article
- Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects particularly motoneurons. Several pieces of evidence suggested the involvement of autoimmune mechanisms mediated by antibodies in ALS. However, the significance of those antibodies in the disease and the underlying mechanisms are unknown. Here we showed that IgG purified from a group of sporadic ALS patients, but not familial ALS patients, specifically interact with the presynaptic membrane of motoneurons through an antigen-antibody interaction and modulated synaptic transmission. Immunoreactivity against nerve terminals showed strong correlation with synaptic modulation ability. In addition, several controls have ruled out the possibility for this synaptic modulation to be mediated through proteases or nonspecific effects. Effective IgG potentiated both spontaneous and asynchronous transmitter release. Application of pharmacological inhibitors suggested that activation of this increased release required a nonconstitutive Ca2+ influx through N-type (Cav2.2) channels and phospholipase C activity and that activation of IP3 and ryanodine receptors were necessary to both activate and sustain the increased release. Consistent with the notion that ALS is heterogeneous disorder, our results reveal that, in approximately 50% of ALS patients, motor nerve terminals constitutes a target for autoimmune response.
Indexed as
Identifiers
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.