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Titolo:
Inhibition of the I-h current in isolated peripheral nerve: A novel mode of peripheral antinociception?
Autore:
Dalle, C; Schneider, M; Clergue, F; Bretton, C; Jirounek, P;
Indirizzi:
Ctr Med Univ Geneva, Dept APSIC Pharmacol, CH-1211 Geneva 4, Switzerland Ctr Med Univ Geneva Geneva Switzerland 4 , CH-1211 Geneva 4, Switzerland Univ Basel, Kantonsspital, Dept Anaesthesia, CH-4031 Basel, Switzerland Univ Basel Basel Switzerland CH-4031 sthesia, CH-4031 Basel, Switzerland
Titolo Testata:
MUSCLE & NERVE
fascicolo: 2, volume: 24, anno: 2001,
pagine: 254 - 261
SICI:
0148-639X(200102)24:2<254:IOTICI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRACHIAL-PLEXUS BLOCK; RAT OPTIC-NERVE; EXCITABILITY CHANGES; INTRAARTICULAR CLONIDINE; DEPENDENT MODULATION; NONMYELINATED NERVE; CUTANEOUS AFFERENTS; MYELINATED AXONS; GANGLION NEURONS; CLAMP ANALYSIS;
Keywords:
activity-dependent hyperpolarization antinociception; clonidine; inward rectification; peripheral nerve; ZD 7288;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Dalle, C Ctr Med Univ Geneva, Dept APSIC Pharmacol, 1 Rue Michel Servet, CH-1211 Geneva 4, Switzerland Ctr Med Univ Geneva 1 Rue Michel Servet Geneva Switzerland 4 and
Citazione:
C. Dalle et al., "Inhibition of the I-h current in isolated peripheral nerve: A novel mode of peripheral antinociception?", MUSCLE NERV, 24(2), 2001, pp. 254-261

Abstract

Although the alpha (2)-adrenergic agonist clonidine has been shown to promote peripheral antinociception, its mechanism of action has not yet been clearly elucidated. By the use of the sucrose-gap method, we have shown that in C fibers of the rabbit vagus nerve, clonidine at micromolar concentrations enhances activity-dependent hyperpolarizations generated by the Na+-K+ pump during and after repetitive stimulation. Similar results were obtained with 10 muM of ZD 7288, a specific blocker of the hyperpolarization-activated cation current (I-h) and with 2 mM of Ba2+ that blocks the inwardly rectifying potassium current (I-KIR). Furthermore, clonidine had no added effect on the ZD 7288-induced response, whereas it produced a marked enhancementof Ba2+-induced response. From these results, it can be concluded that clonidine enhances activity-dependent hyperpolarization by inhibiting the current I-h. We propose that clonidine, by increasing the threshold for initiating the action potential, induces a slowing or block of conduction and thatthis mechanism is the origin of the clonidine-induced antinociception. Finally. this study suggests a novel role for inwardly rectifying hyperpolarization-activated conductances in peripherally mediated antinociception. (C) 2001 John Wiley & Sons, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 09:23:56