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Titolo:
Inositol 1,4,5-triphosphate receptor-sensitive Ca2+ release, store-operated Ca2+ entry, and cAMP responsive element binding protein phosphorylation in developing cortical cells following exposure to polychlorinated biphenyls
Autore:
Inglefield, JR; Mundy, WR; Shafer, TJ;
Indirizzi:
US EPA, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA US EPA Res Triangle Pk NC USA 27711 & Dev, Res Triangle Pk, NC 27711 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 2, volume: 297, anno: 2001,
pagine: 762 - 773
SICI:
0022-3565(200105)297:2<762:I1RCRS>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; PCB MIXTURE AROCLOR-1242; CEREBELLAR GRANULE CELLS; HIPPOCAMPAL-NEURONS; INTRACELLULAR CALCIUM; UTERINE CONTRACTION; RYANODINE RECEPTORS; NEOCORTICAL CELLS; KINASE-C; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Shafer, TJ US EPA, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab,Off Res & Dev, MD-74B, Res Triangle Pk, NC 27711 USA US EPA MD-74B Res Triangle Pk NC USA 27711 gle Pk, NC 27711 USA
Citazione:
J.R. Inglefield et al., "Inositol 1,4,5-triphosphate receptor-sensitive Ca2+ release, store-operated Ca2+ entry, and cAMP responsive element binding protein phosphorylation in developing cortical cells following exposure to polychlorinated biphenyls", J PHARM EXP, 297(2), 2001, pp. 762-773

Abstract

The present study assessed intracellular Ca2+ signaling pathways sensitiveto polychlorinated biphenyls (PCBs), xenobiotics that perturb neural development and plasticity. Mobilization of intracellular Ca2+ stores after acute exposure to a PCB mixture, Aroclor 1254 (A1254), as well as selected PCB congeners, was studied in P0 rat cortical neuronal culture using fluorescence microscopy. Ca2+ responses to A1254 progressed from a transient intracellular Ca2+ increase (lasting 3-5 min) at 1 to 2 muM (0.3-0.6 ppm) to a Ca2transient with store-operated Ca2+ influx and later disturbances of basal Ca2+ concentration; this latter pattern occurred more often with 10 to 20 muM (3-6 ppm) A1254. Thapsigargin, xestospongin C, and carbachol/Ca2+-free buffer blocked significantly the PCB-induced Ca2+ transient, whereas both ryanodine (to deplete ryanodine-sensitive stores) and the L-type Ca2+ channelblocker nifedipine were without effect on the A1254 initial Ca2+ transient. Both thapsigargin and xestospongin also blocked latent elevations (at 0.5h) in Ca2+, disturbances that depend upon extracellular Ca2+ entry via ionchannels. Two possible consequences were explored. Phosphorylation of cAMPresponsive element binding protein, a Ca2+-activated nuclear transcriptionfactor (CREB), occurred in an A1254 concentration-dependent manner and persisted at least 1 h. Cell viability following a 24-h exposure to A1254 (2-20 muM) was decreased at 20 muM, but only in cells cultured >6 days. This cell death did not occur via an apoptotic mechanism. These results indicate that Ca2+ disturbances following PCB exposure are associated with 1) discrete alterations in IP3 receptor-mediated signals and 2) activation of downstream events that impact developing cortical cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 22:36:47