Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Acute actions of tumor necrosis factor-alpha on intracellular Ca2+ and K+ currents in human microglia
Autore:
McLarnon, JG; Franciosi, S; Wang, X; Bae, JH; Choi, HB; Kim, SU;
Indirizzi:
Univ British Columbia, Fac Med, Dept Pharmacol & Therapeut, Vancouver, BC V6T 1Z3, Canada Univ British Columbia Vancouver BC Canada V6T 1Z3 ver, BC V6T 1Z3, Canada Univ British Columbia, Fac Med, Dept Med, Div Neurol, Vancouver, BC V6T 1Z3, Canada Univ British Columbia Vancouver BC Canada V6T 1Z3 ver, BC V6T 1Z3, Canada Keimyung Univ, Sch Med, Taegu, South Korea Keimyung Univ Taegu South Korea myung Univ, Sch Med, Taegu, South Korea Ajou Univ, Brain Dis Res Ctr, Suwon 441749, South Korea Ajou Univ Suwon South Korea 441749 is Res Ctr, Suwon 441749, South Korea
Titolo Testata:
NEUROSCIENCE
fascicolo: 4, volume: 104, anno: 2001,
pagine: 1175 - 1184
SICI:
0306-4522(2001)104:4<1175:AAOTNF>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-TRANSDUCTION PATHWAYS; CULTURED RAT MICROGLIA; TNF-ALPHA; G-PROTEIN; POTASSIUM CURRENTS; GENE-EXPRESSION; ACTIVATION; CELLS; CHANNELS; BRAIN;
Keywords:
human microglia; tumor necrosis factor-alpha; fura-2 spectrofluorometry; intracellular Ca2+; whole-cell patch clamp; K+ current;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: McLarnon, JG Univ British Columbia, Fac Med, Dept Pharmacol & Therapeut, Vancouver, BC V6T 1Z3, Canada Univ British Columbia Vancouver BC Canada V6T1Z3 Z3, Canada
Citazione:
J.G. McLarnon et al., "Acute actions of tumor necrosis factor-alpha on intracellular Ca2+ and K+ currents in human microglia", NEUROSCIENC, 104(4), 2001, pp. 1175-1184

Abstract

The effects of acute application of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF alpha) on levels of intracellular Ca2+ ([Ca2+]i) and on whole-cell outward and inward K+ currents were studied in cultured human microglia. TNF alpha elicited a linear increase in [Ca2+]i to a plateaulevel in microglia bathed in either standard physiological saline solutionor Ca2+-free physiological saline solution. The rate of increase of [Ca2+]i or the level of [Ca2+]i attained was not significantly altered in the absence of external Ca2+ indicating that Ca2+ influx did not contribute appreciably to the cytokine-induced rise in [Ca2-]i. This point was directly confirmed using Mn2+ quenching where no change in signal fluorescence was observed with TNF alpha treatment of microglia in Ca2+-free physiological salinesolution. The rate of increase of [Ca2+]i induced by TNF alpha in Ca2+-free physiological saline solution was not altered by prior application of ATPto deplete inositol triphosphate stores indicating that these stores did not contribute to the cytokine response. In whole-cell patch clamp recordings. the acute treatment of human microglia with TNF alpha led to the expression of an outward K+ current in one-third (14 of 41) of cells. This currentwas activated at potentials positive to -30 mV. showed rapid kinetics of activation with no evident inactivation and had an I-V relation exhibiting outward rectification. Analysis of tail currents showed reversal of the outward K+ current near -70 mV and tetraethylammonium (10 mM) inhibited the outward K+ current to 24% of control level. Acute application of TNF alpha. had no effect to alter inward rectifier currents generated from voltage ramps. The signaling pathways involving TNF alpha modulation of [Ca2+]i and K+ channels in human microglia may contribute to functional and pathological actions of the cytokine in the brain. (C) 2001 IBRO, Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 08:58:54