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Titolo:
mGluR1-mediated potentiation of NMDA receptors involves a rise in intracellular calcium and activation of protein kinase C
Autore:
Skeberdis, VA; Lan, JY; Opitz, T; Zheng, X; Bennett, MVL; Zukin, RS;
Indirizzi:
Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Bronx NY USA 10461 nx, NY 10461 USA
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 7, volume: 40, anno: 2001,
pagine: 856 - 865
SICI:
0028-3908(200106)40:7<856:MPONRI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
METABOTROPIC GLUTAMATE RECEPTORS; CULTURED HIPPOCAMPAL-NEURONS; LONG-TERM POTENTIATION; XENOPUS OOCYTES; SIGNAL-TRANSDUCTION; PHARMACOLOGICAL CHARACTERIZATION; NR1 SUBUNIT; RESPONSES; CURRENTS; PHOSPHORYLATION;
Keywords:
metabotropic glutamate receptors; N-methyl-D-aspartate receptors; phospholipase C; protein kinase C (1S,3R)-ACPD; Xenopus oocytes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Zukin, RS Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, 1300 Morris Pk Ave, Bronx, NY 10461 USA Yeshiva Univ Albert Einstein Coll Med 1300 Morris Pk Ave Bronx NY USA 10461
Citazione:
V.A. Skeberdis et al., "mGluR1-mediated potentiation of NMDA receptors involves a rise in intracellular calcium and activation of protein kinase C", NEUROPHARM, 40(7), 2001, pp. 856-865

Abstract

Potentiation of ionotropic glutamate receptor activity by metabotropic glutamate receptors (mGluRs) is thought to modulate activity at glutamatergic synapses in the hippocampus. However, the precise pathway by which this modulation occurs is not well understood. The present study tests the hypothesis that mGluR1-mediated potentiation of N-methyl-D-aspartate receptors (NMDARs) occurs via a phospholipase C (PLC)-initiated cascade. NMDAR functionalactivity was examined by whole-cell recording from Xenopus oocytes expressing recombinant NMDARs and mGluR1 alpha. The mGluR1 agonist(1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) significantly potentiated NMDA-elicited currents. mGluR1 alpha -mediated potentiation of NMDA responses was eliminated by the PLC inhibitor U-73122. Buffering of intracellular Ca2+ byBAPTA-AM or depletion of intracellular Ca2+ by the Ca2+/ATPase inhibitor thapsigargin greatly reduced ACPD potentiation. ACPD potentiation was reduced by the specific protein kinase C (PKC) inhibitor Ro-32-0432 and eliminated by the broad spectrum kinase inhibitor staurosporine. ACPD produced no further potentiation after potentiation of NMDARs by the PKC-activating phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA). Thus, Group I mGluRs potentiate NMDA responses via activation of PLC; at least part of the potentiation is due to rise in intracellular Ca2+ and stimulation of PKC. Cytochalasin D, which disrupts the actin cytoskeleton, blocked ACPD-elicited chloride currents and ACPD-induced potentiation of NMDAR currents, consistent with a role for cytoskeletal protein(s) in the signaling pathway. As Group ImGluRs are localized to the perisynaptic region in juxtaposition to NMDARsat glutamatergic synapses, mGluR-mediated potentiation of NMDAR activity may play a role in synaptic transmission and plasticity including LTP. (C) 2001 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 05:02:23