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Titolo:
N-methyl D-aspartate receptor-mediated bidirectional control of extracellular signal-regulated kinase activity in cortical neuronal cultures
Autore:
Chandler, LJ; Sutton, G; Dorairaj, NR; Norwood, D;
Indirizzi:
Med Univ S Carolina, Dept Physiol Neurosci, Charleston, SC 29425 USA Med Univ S Carolina Charleston SC USA 29425 sci, Charleston, SC 29425 USA Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA Med Univ S Carolina Charleston SC USA 29425 iat, Charleston, SC 29425 USA Louisiana State Univ, Med Ctr, Dept Pharmacol, Shreveport, LA 71130 USA Louisiana State Univ Shreveport LA USA 71130 ol, Shreveport, LA 71130 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 4, volume: 276, anno: 2001,
pagine: 2627 - 2636
SICI:
0021-9258(20010126)276:4<2627:NDRBCO>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; ELEMENT-BINDING PROTEIN; LONG-TERM-MEMORY; CENTRAL NERVOUS-SYSTEM; MAP KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; SYMPATHETIC NEURONS; CALCIUM INFLUX; CYCLIC-AMP; AREA CA1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Chandler, LJ Med Univ S Carolina, Dept Physiol Neurosci, CDAP IOP 4 N,67 President St, Charleston, SC 29425 USA Med Univ S Carolina CDAP IOP 4 N,67 President St Charleston SC USA 29425
Citazione:
L.J. Chandler et al., "N-methyl D-aspartate receptor-mediated bidirectional control of extracellular signal-regulated kinase activity in cortical neuronal cultures", J BIOL CHEM, 276(4), 2001, pp. 2627-2636

Abstract

N-Methyl D-aspartate (NMDA) receptor activation of extracellular-signal regulated kinase (ERK) was examined in primary cortical cultures. Tetrodotoxin, NMDA receptor antagonists, or reduced extracellular calcium (0.1 mM) greatly decreased basal levels of phospho-ERK2, indicating that activity-dependent activation of NMDA receptors maintained a high level of basal ERK2 activation. This activity-dependent activation of phospho-ERK2 was blocked by pertussis toxin and inhibition of calcium/calmodulin-dependent kinase II and phosphatidylinositol 3-kinase but not by inhibition of protein kinase C or cAMP-dependent protein kinase, Addition of a calcium ionophore or 100 muMNMDA decreased phospho-ERK2 in the presence of 1 mM extracellular calcium but enhanced phospho-ERK2 in 0.1 mM extracellular calcium. The reduction inbasal phospho-ERK2 by 100 muM NMDA was also reflected as a decrease in phospho-cAMP response element-binding protein, Inhibition of tyrosine phosphatases and serine/threonine phosphatases protein phosphatase 1 (PP1), PP2A, and PP2B did not prevent the inhibitory effect of NMDA. In the presence of tetrodotoxin, NMDA produced a bell-shaped dose-response curve with stimulation of phospho-ERK2 at 10, 25, and 50 muM NMDA and reduced stimulation at 100 muM NMDA. NMDA (50 muM) stimulation of phospho-ERK2 was completely blocked by pertussis toxin and inhibitors of phosphatidylinositol 3-kinase and was partially blocked by a calcium/calmodulin-dependent kinase II inhibitor. These results suggests that NMDA receptors can bidirectionally control ERK signaling.

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Documento generato il 02/12/20 alle ore 18:28:28