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A regenerating release of acetylcholine from mouse motor nerve terminals treated with anticholinesterase agents |
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| Authors: | C C Chang S J Hong |
| Affiliation: | 1. Rowett Institute, University of Aberdeen, Ashgrove Rd. West, Aberdeen, AB25 2ZD, UK;2. National Technical University of Ukraine “Igor Sikorsky KPI”, Department of Biotechnology, 37 Beresteiskyi Ave., Kyiv, 03056, Ukraine;3. Odesa National Mechnikov University, Biological Department, 2 Shampansky Ln., Odesa, 65015, Ukraine;1. A.A. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, 4 Bogomoletz Str., Kyiv 01024, Ukraine;2. Educational and Scientific Centre “Institute of Biology and Medicine”, Taras Shevchenko National University of Kyiv, 64 Volodymyrska Str., Kyiv 01601, Ukraine;3. Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom |
| 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. |
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