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Indirect inhibitory effect of succinylcholine on acetylcholine‐activated channel activities and its modulation by external Ca 2+ in mouse skeletal muscles
Author(s) -
Nojima Hiroshi,
Muroi Masashi,
Kimura Masayasu
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14205.x
Subject(s) - chemistry , acetylcholine , acetylcholine receptor , biophysics , extracellular , pipette , patch clamp , conductance , nicotinic acetylcholine receptor , calcium , desensitization (medicine) , nicotinic agonist , membrane potential , endocrinology , receptor , medicine , biochemistry , biology , mathematics , organic chemistry , combinatorics
1 The effect of extracellular calcium on single acetylcholine (ACh)‐activated channel activities when desensitizing concentrations of succinylcholine (SuCh) were applied to the surrounding endplate membrane was investigated by the cell‐attached patch‐clamp technique at endplates of single skeletal muscle (flexor digitorum brevis) fibres of adult mice. 2 Bath‐applied SuCh (0.1–3 μ m , in 2.5 m m Ca 2+ ) increased in a concentration‐dependent manner the mean open time of ACh‐activated channel currents recorded at membrane potentials which cancelled the SuCh‐induced depolarizations. 3 In the presence of 0.5 and 2.5 m m external Ca 2+ , SuCh (3 μ m ) applied outside the patch pipette prolonged the mean open time of ACh‐activated channel currents in a time‐dependent manner (by 45% and 52%, respectively), and simultaneously significantly decreased the single channel conductance (by 14% and 10%, respectively). These SuCh‐induced effects did not occur in a nominally Ca 2+ ‐free extracellular medium. 4 Under the same conditions, SuCh (3 μ m ) augmented the time‐dependent decline in the opening frequency of ACh‐activated channel currents obtained in nominally Ca 2+ ‐free medium. 5 These results suggest that external calcium ions act to modulate nicotinic ACh receptor channel activity, and accelerate desensitization of the receptor.