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Titolo:
Modulation of glycinergic synaptic current kinetics by octanol in mouse hypoglossal motoneurons
Autore:
Oku, Y; Hulsmann, S; Zhang, WQ; Richter, DW;
Indirizzi:
Kyoto Univ, Inst Frontier Med Sci, Dept Med Syst Control, Sakyo Ku, Kyoto 6068397, Japan Kyoto Univ Kyoto Japan 6068397 t Control, Sakyo Ku, Kyoto 6068397, Japan Univ Gottingen, Ctr Physiol & Pathophysiol, Dept Neurophysiol, D-37073 Gottingen, Germany Univ Gottingen Gottingen Germany D-37073 iol, D-37073 Gottingen, Germany
Titolo Testata:
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
fascicolo: 5, volume: 438, anno: 1999,
pagine: 656 - 664
SICI:
0031-6768(199910)438:5<656:MOGSCK>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL NERVOUS-SYSTEM; ACTIVATED CL CURRENT; LONG-CHAIN ALCOHOLS; MAMMALIAN BRAIN; SPINAL NEURONS; RAT; ANESTHETICS; ASTROCYTES; RECEPTORS; EXPRESSION;
Keywords:
gap junction blocker; glycine uptake; intracellular acidification; synaptic transmission;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Oku, Y Kyoto Univ, Inst Frontier Med Sci, Dept Med Syst Control, Sakyo Ku,53 Kawahara Cho, Kyoto 6068397, Japan Kyoto Univ 53 Kawahara Cho Kyoto Japan 6068397 yoto 6068397, Japan
Citazione:
Y. Oku et al., "Modulation of glycinergic synaptic current kinetics by octanol in mouse hypoglossal motoneurons", PFLUG ARCH, 438(5), 1999, pp. 656-664

Abstract

Octanol-induced changes in the kinetics of glycinergic inhibitory postsynaptic currents (IPSCs) were investigated by whole-cell recording from hypoglossal motoneurons in mouse brainstem slices. Octanol (1 mM) prolonged the decay time constants (tau(decay)) of stimulus-evoked IPSCs (e-IPSCs) by 202+/-67% (SE). The depression of e-IPSC amplitudes was dose-dependent with an EC50 of 475 mu M. Octanol also reduced the amplitude and prolonged the decay time constant of glycinergic currents evoked by local pressure ejection of glycine (I-gly). Replacement of extracellular Na+ by choline and application of the specific glycine transporter GLYT1 inhibitor, sarcosine, lengthened tau(decay) of I-gly, but did not change the decay time constants of e-IPSCs. Intracellular acidification by the weak organic acid salt sodium propionate (30 mM) reduced the e-IPSC amplitude by 22+/-9% and prolonged tau by18+/-6%. Sodium propionate also prolonged the decay time constants of I-gly by 28+/-11%. The observed effects on decay kinetics were much smaller than those caused by octanol. The data show that octanol prolongs the decay time course of glycinergic synaptic currents by mechanisms independent of glycine uptake or intracellular acidification. We conclude that the effects were most probably due to direct action on postsynaptic glycine receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 15:49:28