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This Article Full Text Full Text (PDF) All Versions of this Article: 560/1/77    most recent jphysiol.2004.065805v2 jphysiol.2004.065805v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Nikolsky, E. E Articles by Magazanik, L. G Search for Related Content PubMed PubMed Citation Articles by Nikolsky, E. E Articles by Magazanik, L. G

Eugeny E Nikolsky^1,2, Frantiek Vyskoil³, Ella A Bukharaeva^1,2, Dmitry Samigullin¹ and Lev G Magazanik⁴

¹ Institute of Biochemistry and Biophysics, Russian Academy of Sciences, PO Box 30, Kazan, Russia
² State Medical University, Butlerov st. 49, Kazan, Russia
³ Department of Animal Physiology and Developmental Biology, Faculty of Sciences, Charles University, Viniá 7, Prague 2 and Institute of Physiology, Academy of Sciences of the Czech Republic, Vídeská 1083, Prague 4, Czech Republic
⁴ I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, Thorez pr., 44, St Petersburg, 194223 Russia

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 x 10^–4 M), carbachol (CCh, 1 x 10^–5 M) or nicotine (5 x 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 x 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.

(Received 2 April 2004; accepted after revision 8 July 2004; first published online 14 July 2004)
Corresponding author F. Vyskoil: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídeská 1083, Prague 4, 142 20 Czech Republic. Email: vyskocil{at}biomed.cas.cz