Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker
In order to search for early changes induced by the application of human immunoglobulin G (IgG) on motor nerve terminals, IgG from patients with amyotrophic lateral sclerosis (ALS) and control subjects was injected subcutaneously into the levator auris muscle of mice. A week or a month after the las...
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2000
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0148639X_v23_n4_p543_Fratantoni http://hdl.handle.net/20.500.12110/paper_0148639X_v23_n4_p543_Fratantoni |
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paper:paper_0148639X_v23_n4_p543_Fratantoni2023-06-08T15:13:11Z Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker Amyotrophic lateral sclerosis Calcium channels Neuromuscular junction Nitrendipine Transmitter release calcium channel blocking agent immunoglobulin G nitrendipine adult aged amyotrophic lateral sclerosis animal cell animal model animal tissue article calcium transport clinical article controlled study female human human cell human tissue immunotherapy male mouse nerve cell necrosis neurotransmitter release nonhuman priority journal protein expression voltage clamp Adult Aged Animals Calcium Channel Blockers Calcium Channels, L-Type Evoked Potentials Female Humans Immunoglobulin G Male Mice Middle Aged Motor Neuron Disease Muscle, Skeletal Neuromuscular Junction Nitrendipine omega-Agatoxin IVA omega-Conotoxin GVIA Reference Values In order to search for early changes induced by the application of human immunoglobulin G (IgG) on motor nerve terminals, IgG from patients with amyotrophic lateral sclerosis (ALS) and control subjects was injected subcutaneously into the levator auris muscle of mice. A week or a month after the last injection, endplate potentials were recorded. No changes in quantal content of transmitter release were observed. In control and ALS IgG-treated muscles, neurotransmitter release remained sensitive to P/Q-type and insensitive to N-type voltage-sensitive calcium channel (VSCC) blockers as in untreated muscles. In contrast, IgG from 5 of 8 different ALS patients induced a significant reduction in quantal content of the evoked response after incubation with nitrendipine, indicating that a novel sensitivity to this calcium channel blocker appears in these motor nerve terminals. These results indicate that ALS IgG induces plastic changes at nerve terminals. The expression of transmitter release coupled to L-type VSCC indicate that ALS IgGs are capable of inducing plastic changes at the nerve terminals that may participate in the process leading to neuronal death. (C) 2000 John Wiley and Sons, Inc. 2000 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0148639X_v23_n4_p543_Fratantoni http://hdl.handle.net/20.500.12110/paper_0148639X_v23_n4_p543_Fratantoni |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Amyotrophic lateral sclerosis Calcium channels Neuromuscular junction Nitrendipine Transmitter release calcium channel blocking agent immunoglobulin G nitrendipine adult aged amyotrophic lateral sclerosis animal cell animal model animal tissue article calcium transport clinical article controlled study female human human cell human tissue immunotherapy male mouse nerve cell necrosis neurotransmitter release nonhuman priority journal protein expression voltage clamp Adult Aged Animals Calcium Channel Blockers Calcium Channels, L-Type Evoked Potentials Female Humans Immunoglobulin G Male Mice Middle Aged Motor Neuron Disease Muscle, Skeletal Neuromuscular Junction Nitrendipine omega-Agatoxin IVA omega-Conotoxin GVIA Reference Values |
| spellingShingle |
Amyotrophic lateral sclerosis Calcium channels Neuromuscular junction Nitrendipine Transmitter release calcium channel blocking agent immunoglobulin G nitrendipine adult aged amyotrophic lateral sclerosis animal cell animal model animal tissue article calcium transport clinical article controlled study female human human cell human tissue immunotherapy male mouse nerve cell necrosis neurotransmitter release nonhuman priority journal protein expression voltage clamp Adult Aged Animals Calcium Channel Blockers Calcium Channels, L-Type Evoked Potentials Female Humans Immunoglobulin G Male Mice Middle Aged Motor Neuron Disease Muscle, Skeletal Neuromuscular Junction Nitrendipine omega-Agatoxin IVA omega-Conotoxin GVIA Reference Values Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| topic_facet |
Amyotrophic lateral sclerosis Calcium channels Neuromuscular junction Nitrendipine Transmitter release calcium channel blocking agent immunoglobulin G nitrendipine adult aged amyotrophic lateral sclerosis animal cell animal model animal tissue article calcium transport clinical article controlled study female human human cell human tissue immunotherapy male mouse nerve cell necrosis neurotransmitter release nonhuman priority journal protein expression voltage clamp Adult Aged Animals Calcium Channel Blockers Calcium Channels, L-Type Evoked Potentials Female Humans Immunoglobulin G Male Mice Middle Aged Motor Neuron Disease Muscle, Skeletal Neuromuscular Junction Nitrendipine omega-Agatoxin IVA omega-Conotoxin GVIA Reference Values |
| description |
In order to search for early changes induced by the application of human immunoglobulin G (IgG) on motor nerve terminals, IgG from patients with amyotrophic lateral sclerosis (ALS) and control subjects was injected subcutaneously into the levator auris muscle of mice. A week or a month after the last injection, endplate potentials were recorded. No changes in quantal content of transmitter release were observed. In control and ALS IgG-treated muscles, neurotransmitter release remained sensitive to P/Q-type and insensitive to N-type voltage-sensitive calcium channel (VSCC) blockers as in untreated muscles. In contrast, IgG from 5 of 8 different ALS patients induced a significant reduction in quantal content of the evoked response after incubation with nitrendipine, indicating that a novel sensitivity to this calcium channel blocker appears in these motor nerve terminals. These results indicate that ALS IgG induces plastic changes at nerve terminals. The expression of transmitter release coupled to L-type VSCC indicate that ALS IgGs are capable of inducing plastic changes at the nerve terminals that may participate in the process leading to neuronal death. (C) 2000 John Wiley and Sons, Inc. |
| title |
Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| title_short |
Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| title_full |
Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| title_fullStr |
Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| title_full_unstemmed |
Amyotrophic lateral sclerosis IgG-treated neuromuscular junctions develop sensitivity to L-type calcium channel blocker |
| title_sort |
amyotrophic lateral sclerosis igg-treated neuromuscular junctions develop sensitivity to l-type calcium channel blocker |
| publishDate |
2000 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0148639X_v23_n4_p543_Fratantoni http://hdl.handle.net/20.500.12110/paper_0148639X_v23_n4_p543_Fratantoni |
| _version_ |
1768541603748642816 |