Monoclonal antibody to β2 subunit of neuronal nicotinic receptor depresses the postjunctional non-contractile Ca2+ mobilization in the mouse diaphragm muscle

Ikuko Kimura; Hiroshi Tsuneki; Katsuya Dezaki; Hiroshi Nojima; Masayasu Kimura

doi:10.1016/0304-3940(94)90497-9

Monoclonal antibody to β2 subunit of neuronal nicotinic receptor depresses the postjunctional non-contractile Ca²⁺ mobilization in the mouse diaphragm muscle

Ikuko Kimura^*, Hiroshi Tsuneki, Katsuya Dezaki, Hiroshi Nojima, Masayasu Kimura

^*Corresponding author for this work

Integrative Pharmacology

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

The involvement of subtypes of nicotinic acetylcholine receptor (nAChR) in the postjunctional non-contractile Ca²⁺ mobilization was investigated in mouse diaphragm muscles treated with an anticholinesterase, using monoclonal antibodies (mAbs) to nAChR subunits. mAb 210 (specific for α1 subunit of muscle nAChR) depressed contractile Ca²⁺ transients without affecting non-contractile Ca²⁺ transients. mAb 270 (specific for β2 subunit of neuronal nAChR) depressed only non-contractile Ca²⁺ transients. mAb 210 did not completely block the ACh-activated channel currents in flexor digitorum brevis muscle cells. The present findings indicate that the anti-β2 mAb 270-related subtype of nAChR may postsynaptically operate the non-contractile Ca²⁺ mobilization at the neuromuscular junction, suggesting the involvement of a subtype different from the usual muscle-type nAChR.

Original language	English
Pages (from-to)	101-104
Number of pages	4
Journal	Neuroscience Letters
Volume	180
Issue number	2
DOIs	https://doi.org/10.1016/0304-3940(94)90497-9
State	Published - 1994/10/24

Keywords

Calcium
Monoclonal antibody
Neuromuscular junction
Nicotinic acetylcholine receptor

ASJC Scopus subject areas

General Neuroscience

Access to Document

10.1016/0304-3940(94)90497-9

Cite this

@article{a8380e257ae24f119d117ab16f499778,

title = "Monoclonal antibody to β2 subunit of neuronal nicotinic receptor depresses the postjunctional non-contractile Ca2+ mobilization in the mouse diaphragm muscle",

abstract = "The involvement of subtypes of nicotinic acetylcholine receptor (nAChR) in the postjunctional non-contractile Ca2+ mobilization was investigated in mouse diaphragm muscles treated with an anticholinesterase, using monoclonal antibodies (mAbs) to nAChR subunits. mAb 210 (specific for α1 subunit of muscle nAChR) depressed contractile Ca2+ transients without affecting non-contractile Ca2+ transients. mAb 270 (specific for β2 subunit of neuronal nAChR) depressed only non-contractile Ca2+ transients. mAb 210 did not completely block the ACh-activated channel currents in flexor digitorum brevis muscle cells. The present findings indicate that the anti-β2 mAb 270-related subtype of nAChR may postsynaptically operate the non-contractile Ca2+ mobilization at the neuromuscular junction, suggesting the involvement of a subtype different from the usual muscle-type nAChR.",

keywords = "Calcium, Monoclonal antibody, Neuromuscular junction, Nicotinic acetylcholine receptor",

author = "Ikuko Kimura and Hiroshi Tsuneki and Katsuya Dezaki and Hiroshi Nojima and Masayasu Kimura",

note = "Funding Information: We thank Prof. J. Lindstrom (University of Pennsylvania) and Prof. D.K. Berg (University of California, San Diego) lbr providing all the mAbs used in the present study and for helpful comments. This work was supported by Grant-in-Aid for JSPS Fellows (No. 061200) from the Ministry of Education, Science and Culture, Japan.",

year = "1994",

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doi = "10.1016/0304-3940(94)90497-9",

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T1 - Monoclonal antibody to β2 subunit of neuronal nicotinic receptor depresses the postjunctional non-contractile Ca2+ mobilization in the mouse diaphragm muscle

AU - Kimura, Ikuko

AU - Tsuneki, Hiroshi

AU - Dezaki, Katsuya

AU - Nojima, Hiroshi

AU - Kimura, Masayasu

N1 - Funding Information: We thank Prof. J. Lindstrom (University of Pennsylvania) and Prof. D.K. Berg (University of California, San Diego) lbr providing all the mAbs used in the present study and for helpful comments. This work was supported by Grant-in-Aid for JSPS Fellows (No. 061200) from the Ministry of Education, Science and Culture, Japan.

PY - 1994/10/24

Y1 - 1994/10/24

N2 - The involvement of subtypes of nicotinic acetylcholine receptor (nAChR) in the postjunctional non-contractile Ca2+ mobilization was investigated in mouse diaphragm muscles treated with an anticholinesterase, using monoclonal antibodies (mAbs) to nAChR subunits. mAb 210 (specific for α1 subunit of muscle nAChR) depressed contractile Ca2+ transients without affecting non-contractile Ca2+ transients. mAb 270 (specific for β2 subunit of neuronal nAChR) depressed only non-contractile Ca2+ transients. mAb 210 did not completely block the ACh-activated channel currents in flexor digitorum brevis muscle cells. The present findings indicate that the anti-β2 mAb 270-related subtype of nAChR may postsynaptically operate the non-contractile Ca2+ mobilization at the neuromuscular junction, suggesting the involvement of a subtype different from the usual muscle-type nAChR.

AB - The involvement of subtypes of nicotinic acetylcholine receptor (nAChR) in the postjunctional non-contractile Ca2+ mobilization was investigated in mouse diaphragm muscles treated with an anticholinesterase, using monoclonal antibodies (mAbs) to nAChR subunits. mAb 210 (specific for α1 subunit of muscle nAChR) depressed contractile Ca2+ transients without affecting non-contractile Ca2+ transients. mAb 270 (specific for β2 subunit of neuronal nAChR) depressed only non-contractile Ca2+ transients. mAb 210 did not completely block the ACh-activated channel currents in flexor digitorum brevis muscle cells. The present findings indicate that the anti-β2 mAb 270-related subtype of nAChR may postsynaptically operate the non-contractile Ca2+ mobilization at the neuromuscular junction, suggesting the involvement of a subtype different from the usual muscle-type nAChR.

KW - Calcium

KW - Monoclonal antibody

KW - Neuromuscular junction

KW - Nicotinic acetylcholine receptor

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