ArticleProceedings of the National Academy of Sciences of the United States of America1993
IgG from amyotrophic lateral sclerosis patients increases current through P-type calcium channels in mammalian cerebellar Purkinje cells and in isolated channel protein in lipid bilayer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 97 citations in OpenAlex.
- Passive Transfer of Blood Sera from ALS Patients with Identified Mutations Results in Elevated Motoneuronal Calcium Level and Loss of Motor Neurons in the Spinal Cord of Mice.International journal of molecular sciences · 2021Article
- Passive Transfer of Sera from ALS Patients with Identified Mutations Evokes an Increased Synaptic Vesicle Number and Elevation of Calcium Levels in Motor Axon Terminals, Similar to Sera from Sporadic Patients.International journal of molecular sciences · 2020Article
- 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
- Novel molecular biomarkers at the blood-brain barrier in ALS.BioMed research international · 2014Review
- Autoimmunity in amyotrophic lateral sclerosis: past and present.Neurology research international · 2011Article
- Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease.BMC neuroscience · 2009Article
- Calcium signaling pathways mediating synaptic potentiation triggered by amyotrophic lateral sclerosis IgG in motor nerve terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Single-cell RT-PCR and functional characterization of Ca2+ channels in motoneurons of the rat facial nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Immunoglobulins from motoneurone disease patients enhance glutamate release from rat hippocampal neurones in culture.The Journal of physiology · 1997Article
- Differential localization of voltage-dependent calcium channel alpha1 subunits at the human and rat neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Cytotoxicity of immunoglobulins from amyotrophic lateral sclerosis patients on a hybrid motoneuron cell line.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The effect of the IgG from amyotrophic lateral sclerosis (ALS) patients was tested on the voltage-dependent barium currents (IBa) in mammalian dissociated Purkinje cells and in isolated P-type calcium channels in lipid bilayers. Whole cell clamp of Purkinje cells demonstrates that ALS IgG increases the amplitude of IBa without modifying their voltage kinetics. This increased IBa could be blocked by a purified nonpeptide toxin from Agelenopsis aperta venom (purified funnel-web spider toxin) or by a synthetic polyamine analog (synthetic funnel-web spider toxin) and by a peptide toxin from the same spider venom, omega-Aga-IVA. Similar results were obtained on single-channel recordings from purified P channel protein. The addition of ALS IgG increased single-channel IBa open time without affecting slope conductance. The results described above were not seen with normal human IgG nor with boiled ALS IgG. It is concluded that ALS IgG enhances inward current through P-type calcium channels. Since P-type Ca2+ channels are present in motoneuron axon terminals, we propose that the enhanced calcium current triggered by ALS IgG may contribute to neuronal damage in ALS.
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