Cholinergic regulation of the evoked quantal release at frog neuromuscular junction

Authors

  • Eugeny E. Nikolsky,

    1. Institute of Biochemistry and Biophysics, Russian Academy of Sciences, PO Box 30, Kazan, Russia
    2. State Medical University, Butlerov st. 49, Kazan, Russia
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  • František Vyskočil,

    1. Department of Animal Physiology and Developmental Biology, Faculty of Sciences, Charles University, Viničá 7, Prague 2 and Institute of Physiology, Academy of Sciences of the Czech Republic, Vídeňská 1083, Prague 4, Czech Republic
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  • Ella A. Bukharaeva,

    1. Institute of Biochemistry and Biophysics, Russian Academy of Sciences, PO Box 30, Kazan, Russia
    2. State Medical University, Butlerov st. 49, Kazan, Russia
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  • Dmitry Samigullin,

    1. Institute of Biochemistry and Biophysics, Russian Academy of Sciences, PO Box 30, Kazan, Russia
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  • Lev G. Magazanik

    1. I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, Thorez pr., 44, St Petersburg, 194223 Russia
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Corresponding author F. Vyskočil: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídeňská 1083, Prague 4, 142 20 Czech Republic. Email: vyskocil@biomed.cas.cz

Abstract

The effects of cholinergic drugs on the quantal contents of the nerve-evoked endplate currents (EPCs) and the parameters of the time course of quantal release (minimal synaptic latency, main modal value of latency histogram and variability of synaptic latencies) were studied at proximal, central and distal regions of the frog neuromuscular synapse. Acetylcholine (ACh, 5 × 10−4m), carbachol (CCh, 1 × 10−5m) or nicotine (5 × 10−6m) increased the numbers of EPCs with long release latencies mainly in the distal region of the endplate (90–120 μm from the last node of Ranvier), where the synchronization of transmitter release was the most pronounced. The parameters of focally recorded motor nerve action potentials were not changed by either ACh or CCh. The effects of CCh and nicotine on quantal dispersion were reduced substantially by 5 × 10−7m (+)tubocurarine (TC). The muscarinic agonists, oxotremorine and the propargyl ester of arecaidine, as well as antagonists such as pirenzepine, AF-DX 116 and methoctramine, alone or in combination, did not affect the dispersion of the release. Muscarinic antagonists did not block the dispersion action of CCh. Cholinergic drugs either decreased the quantal content mo (muscarinic agonist, oxotremorine M, and nicotinic antagonist, TC), or decreased mo and dispersed the release (ACh, CCh and nicotine). The effects on mo were not related either to the endplate region or to the initial level of release dispersion. It follows that the mechanisms regulating the amount and the time course of transmitter release are different and that, among other factors, they are altered by presynaptic nicotinic receptors.

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