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Titolo:
THE EFFECT OF ACETYLCHOLINE AND RELATED DRUGS ON CURRENTS AT THE FROGMOTOR-NERVE TERMINAL
Autore:
SHAKIRYANOVA DM; ZEFIROV AL; NIKOLSKY EE; VYSKOCIL F;
Indirizzi:
KAZAN MED UNIV,BUTLEROVA 49 KAZAN 420012 RUSSIA KAZAN MED UNIV KAZAN 420012 RUSSIA KAZAN INST BIOL KAZAN 420111 RUSSIA ACAD SCI CZECH REPUBL,INST PHYSIOL CR-14220 PRAGUE CZECH REPUBLIC
Titolo Testata:
European journal of pharmacology
fascicolo: 1-2, volume: 263, anno: 1994,
pagine: 107 - 114
SICI:
0014-2999(1994)263:1-2<107:TEOAAR>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOUSE HEMIDIAPHRAGM PREPARATION; PLATE POTENTIAL FREQUENCY; NA+-K+-ATPASE; TRANSMITTER RELEASE; NEUROMUSCULAR-JUNCTION; PRESYNAPTIC MODULATION; EVOKED RELEASE; CURARE; IONS; TRANSMISSION;
Keywords:
NERVE TERMINAL CURRENT; CHOLINOMIMETIC; ACETYLCHOLINE; ANTICHOLINESTERASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
D.M. Shakiryanova et al., "THE EFFECT OF ACETYLCHOLINE AND RELATED DRUGS ON CURRENTS AT THE FROGMOTOR-NERVE TERMINAL", European journal of pharmacology, 263(1-2), 1994, pp. 107-114

Abstract

Acetylcholine, acetylthiocholine, carbachol, suberyldicholine, propionylcholine, succinylcholine, methylfurmethide and F 2268 were tested on motor nerve ending currents recorded with an extracellular microelectrode. The isolated and transversally cut cutaneus pectoris muscle of frog Rana ridibunda was used. Only acetylcholine and acetylthiocholineaffected the spike waveforms in a concentration-dependent manner. Lower concentrations (1-6 x 10(-4) M) prolonged the inward Na+ current and increased the outward K+ current at the proximal and central parts of the nerve terminal. Most remote parts of the terminal were not affected. At 7 x 10(-4) M and higher, both drugs further prolonged the Na+ current and eliminated the K+ component of the spike. The potentiatingeffect of acetylcholine and acetylthiocholine on the K+ phase of nerve terminal current disappeared after treatment with tetraethylammoniumand 4-aminopyridine. The effect also disappeared when synaptic cholinesterase was inhibited by the anticholinesterases or by treatment withcollagenase. Reactivation of cholinesterase by dipyroxime restored the facilitating effect of acetylcholine. Choline and slight acidification to pH 6.8 did not mimic the acetylcholine action on the terminal currents. Facilitation of the K+ current by acetylcholine was not calcium-dependent. The results indicate that lower acetylcholine concentrations inhibit the delayed rectifier only, whereas 7 x 10(-4) M and higher concentrations of acetylcholine depress all outward currents of the terminal.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 03:51:41