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Titolo:
ACTIVATION OF A METABOTROPIC EXCITATORY AMINO-ACID RECEPTOR POTENTIATES SPIKE-DRIVEN CALCIUM INCREASES IN NEURONS OF THE DORSOLATERAL SEPTUM
Autore:
ZHENG F; GALLAGHER JP; CONNOR JA;
Indirizzi:
EMORY UNIV,SCH MED,DEPT PHARMACOL,1510 CLIFTON RD ATLANTA GA 30322 ROCHE INST MOL BIOL NUTLEY NJ 07110 UNIV TEXAS,MED BRANCH,DEPT PHARMACOL & TOXICOL GALVESTON TX 77555 LOVELACE BIOMED & ENVIRONM RES INST ALBUQUERQUE NM 87105
Titolo Testata:
The Journal of neuroscience
fascicolo: 19, volume: 16, anno: 1996,
pagine: 6079 - 6088
SICI:
0270-6474(1996)16:19<6079:AOAMEA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
MGLUR1 MUTANT MICE; TRANS-ACPD; NUCLEUS; THAPSIGARGIN; INHIBITION; INVITRO; BRAIN; MOBILIZATION; CA1;
Keywords:
METABOTROPIC GLUTAMATE RECEPTORS; INTRACELLULAR CALCIUM; LONG-TERM POTENTIATION; NEUROTOXICITY; THAPSIGARGIN; RYANODINE; VOLTAGE-GATED CALCIUM CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
F. Zheng et al., "ACTIVATION OF A METABOTROPIC EXCITATORY AMINO-ACID RECEPTOR POTENTIATES SPIKE-DRIVEN CALCIUM INCREASES IN NEURONS OF THE DORSOLATERAL SEPTUM", The Journal of neuroscience, 16(19), 1996, pp. 6079-6088

Abstract

(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), an agonist for metabotropic glutamate receptors (mGluRs), causes depolarization and burst firing in rat dorsolateral septal nucleus (DLSN) neurons and results in long-term potentiation (LTP) at DLSN synapses. In thepresent study, we investigated whether these actions of 1S,3R-ACPD are attributable to the release of calcium from an inositol triphosphate-sensitive store after activation of mGluRs coupled to phospholipase C. Our data demonstrated that the ACPD-induced depolarization was associated with a small but significant decrease, not an increase, in [Ca2+](i); however, changes of [Ca2+](i) during ACPD-induced bursting were up to seven times larger than those produced by regular firing. Depletion of internal calcium stores by thapsigargin or ryanodine had a small to insignificant effect on the maximum changes of [Ca2+](i) associated with ACPD-induced bursting. Thus, elevation of [Ca2+](i) during firing by 1S,3R-ACPD is likely attributable to enhancement of calcium influx through voltage-gated channels and not to calcium release from internal stores. ACPD-induced burst firing elevated somatic and dendriticcalcium levels up to 3 and 6 mu M, respectively. Such an increase maybe the underlying mechanism for ACPD-induced LTP as well as ACPD-induced acute cell death in rat DLSN.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:52:09