Cholinergic regulation of the evoked quantal release at frog neuromuscular junction

• Published in: The Journal of physiology 2004-10, Vol.560 (1), p.77-88
• Main Authors: Nikolsky, Eugeny E., Vyskočil, František, Bukharaeva, Ella A., Samigullin, Dmitry, Magazanik, Lev G.
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Action Potentials - drug effects; Action Potentials - physiology; Animals; Anura; Arecoline - analogs & derivatives; Arecoline - pharmacology; Carbachol - pharmacology; Cholinergic Agonists - pharmacology; Diamines - pharmacology; Motor Neurons - physiology; Muscarinic Agonists - pharmacology; Muscarinic Antagonists - pharmacology; Neural Conduction - drug effects; Neural Conduction - physiology; Neuromuscular Junction - drug effects; Neuromuscular Junction - physiology; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; Nicotinic Antagonists - pharmacology; Oxotremorine - analogs & derivatives; Oxotremorine - pharmacology; Parasympatholytics - pharmacology; Pirenzepine - analogs & derivatives; Pirenzepine - pharmacology; Rana ridibunda; Receptors, Muscarinic - physiology; Research Papers; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Tubocurarine - pharmacology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2004.065805

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 −4 m ), carbachol (CCh, 1 × 10 −5 m ) or nicotine (5 × 10 −6 m ) 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 −7 m (+)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 m o (muscarinic agonist, oxotremorine M, and nicotinic antagonist, TC), or decreased m o and dispersed the release (ACh, CCh and nicotine). The effects on m o 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.