PMID: 3763048Aug 29, 1986Paper

A regenerating release of acetylcholine from mouse motor nerve terminals treated with anticholinesterase agents

Neuroscience Letters
C C Chang, S J Hong

Abstract

It was found by intracellular recording with glass microelectrodes that train stimulation (50-200 Hz) of the phrenic nerve of intact or cut mouse diaphragm induced an accumulative depolarization of the endplate and triggered after a few pulses an 'all-or-none' regenerative depolarization lasting for 300-900 ms when acetylcholinesterase was inhibited by neostigmine or diisopropylfluorophosphate. This depolarization was associated with a noise of the membrane potential and a failure of the end plate potential. Low Ca2+ prolonged whereas high Ca2+ shortened the duration of regenerative depolarization which needed no further stimulation once triggered. d-Tubocurarine abolished the depolarization while restoring the end plate potential. A regenerative release of acetylcholine due to an activation of presynaptic cholinoceptors is speculated.

References

Sep 1, 1978·The Journal of Cell Biology·J del Castillo, G Escalona de Motta
Apr 1, 1986·British Journal of Pharmacology·C C ChangJ L Ko
Jan 1, 1983·Annual Review of Physiology·R W Tsien

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Citations

Jun 5, 1992·European Journal of Pharmacology·L C Chiou, C C Chang
Jan 1, 1992·Progress in Neurobiology·M Scuka, J W Mozrzymas
Oct 2, 1990·Neuroscience Letters·A Deana, M Scuka
Jan 13, 1995·European Journal of Pharmacology·L C ChiouC C Chang
Aug 1, 1994·Acta Anaesthesiologica Scandinavica·W C Bowman
Dec 1, 1990·British Journal of Pharmacology·S J Hong, C C Chang
May 1, 1992·British Journal of Pharmacology·S Y Lin-ShiauW M Fu
Jan 1, 1990·Annals of the New York Academy of Sciences·W C BowmanI G Marshall
Nov 5, 1999·Journal of Biomedical Science·C C Chang
May 15, 2021·Clinical Toxicology : the Official Journal of the American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists·Kosala N DissanayakeRichard R Ribchester

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