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Titolo:
Isoflurane slows inactivation kinetics of rat recombinant alpha(1)beta(2)gamma(2L) GABA(A) receptors: enhancement of GABAergic transmission despite an open-channel block
Autore:
Hapfelmeier, G; Haseneder, R; Eder, M; Adelsberger, H; Kochs, E; Rammes, G; Zieglgansberger, W;
Indirizzi:
Tech Univ Munich, Klinikum Rechts Isar, Dept Anesthesiol, D-8000 Munich, Germany Tech Univ Munich Munich Germany D-8000 esthesiol, D-8000 Munich, Germany Max Planck Inst Psychiat, D-8000 Munich, Germany Max Planck Inst PsychiatMunich Germany D-8000 t, D-8000 Munich, Germany Univ Munich, Inst Zool, D-8000 Munich, Germany Univ Munich Munich Germany D-8000 ich, Inst Zool, D-8000 Munich, Germany
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 2, volume: 307, anno: 2001,
pagine: 97 - 100
SICI:
0304-3940(20010713)307:2<97:ISIKOR>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHLORIDE CHANNEL; VOLATILE ANESTHETICS; HIPPOCAMPAL-NEURONS; CRAYFISH; CURRENTS; MEMBRANE; MUSCLE; IPSCS;
Keywords:
gamma-aminobutyric acid (A) receptor; channel block; patch-clamp; anesthetics; isoflurane; computer simulations;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
16
Recensione:
Indirizzi per estratti:
Indirizzo: Hapfelmeier, G Tech Univ Munich, Klinikum Rechts Isar, Dept Anesthesiol, D-8000 Munich, Germany Tech Univ Munich Munich Germany D-8000 00 Munich, Germany
Citazione:
G. Hapfelmeier et al., "Isoflurane slows inactivation kinetics of rat recombinant alpha(1)beta(2)gamma(2L) GABA(A) receptors: enhancement of GABAergic transmission despite an open-channel block", NEUROSCI L, 307(2), 2001, pp. 97-100

Abstract

Recombinant alpha (1)beta (2)gamma (2L) gamma -aminobutyric acid (A) receptor (GABA(A)R) channels expressed in human embryonic kidney (HEK293) cells were used for patch-clamp experiments. The currents activated by brief pulses of GABA (10(-4) M) applied with a device for fast solution exchange to cells clamped in the whole-cell configuration mimicked GABA(A)R-mediated inhibitory postsynaptic currents. Isoflurane (ISO) at clinically relevant concentrations (0.6 mM) decreased the amplitude and prolonged the decay of the GABA-evoked response. To further detail the mechanism underlying the prolonged decay time, we made simulations based on these measurements. These simulations suggest that ISO slows the rate of GABA unbinding from the receptor. Under these conditions, ISO increases the GABA-induced charge transfer and, thus, could enhance GABAergic inhibition despite the concomitant open-channel block causing the decrease in the current amplitude. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

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Documento generato il 09/04/20 alle ore 10:17:16