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Titolo:
FORSKOLIN AND PHORBOL-MYRISTATE ACETATE INHIBIT INTRACELLULAR CA2+ MOBILIZATION INDUCED BY AMITRIPTYLINE AND BRADYKININ IN RAT FRONTOCORTICAL NEURONS
Autore:
SHIMIZU M; NISHIDA A; YAMAWAKI S;
Indirizzi:
KURE NATL HOSP,INST CLIN RES,DEPT PSYCHIAT & NEUROSCI,3-1 AOYAMA KURE737 JAPAN
Titolo Testata:
Journal of neurochemistry
fascicolo: 5, volume: 61, anno: 1993,
pagine: 1748 - 1754
SICI:
0022-3042(1993)61:5<1748:FAPAII>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; HYBRID NG108-15 CELLS; 1,4,5-TRISPHOSPHATE-INDUCED CA-2+ RELEASE; AMP-DEPENDENT PHOSPHORYLATION; GATED K+ CHANNELS; CYCLIC-AMP; PHOSPHOINOSITIDE TURNOVER; CALCIUM MOBILIZATION; INOSITOL PHOSPHATES; SIGNAL TRANSDUCTION;
Keywords:
AMITRIPTYLINE; BRADYKININ; CA2+ MOBILIZATION; FORSKOLIN; INOSITOL 1,4,5-TRISPHOSPHATE; PHORBOL ESTER; RAT BRAIN CULTURED NEURONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
M. Shimizu et al., "FORSKOLIN AND PHORBOL-MYRISTATE ACETATE INHIBIT INTRACELLULAR CA2+ MOBILIZATION INDUCED BY AMITRIPTYLINE AND BRADYKININ IN RAT FRONTOCORTICAL NEURONS", Journal of neurochemistry, 61(5), 1993, pp. 1748-1754

Abstract

Regulations of the increase in intracellular Ca2+ concentration ([Ca2]i) and inositol 1,4,5-trisphosphate (IP3) production by increasing intracellular cyclic AMP (cAMP) levels or activating protein kinase C (PKC) were studied in rat frontocortical cultured neurons. Amitriptyline (AMI; 1 mM), a tricyclic antidepressant, and bradykinin (BK; 1 muM) stimulated IP3 production and caused transient [Ca2+]i increases. Pretreatment with forskolin (100 muM, 15 min) decreased the AMI- and BK-induced [Ca2+]i increases by 33 and 48%, respectively. However, this treatment had no effect on the AMI- and BK-induced IP3 productions. Dibutyryl-cAMP (2 mM, 15 min) also decreased the AMI- and BK-induced [Ca2+]i increases by 23 and 47%, respectively. H-8 (30 muM), an inhibitor ofprotein kinase A (PKA), attenuated the ability of forskolin to inhibit the AMI- and BK-induced [Ca2+]i, increases, suggesting that the activation of cAMP/PKA was involved in these inhibitory effects of forskolin. On the other hand, forskolin treatment had no effect on 20 mM caffeine-, 10 muM glutamate-, or 50 mM K+-induced [Ca2+]i increases. Pretreatment with phorbol 12-myristate 13-acetate (PMA; 100 nM, 90 min) decreased both the AMI-induced [Ca2+]i increases and the IP3 production by 31 and 25%, respectively. H-7 (200 muM), an inhibitor of PKC, inhibited the ability of PMA to attenuated the [Ca2+]i increases. PMA also inhibited the BK-induced IP3 production and the [Ca2+]i increases. Taken together, these results suggest that activation of cAMP/PKA may inhibit the IP,-mediated Ca2+ release from internal stores; on the other hand, activation of PKC may inhibit the phosphatidylinositol 4,5-bisphosphate breakdown and consequently reduce the [Ca2+]i increases or inhibit independently both responses. PKA and PKC may differently regulatethe phosphatidylinositol-Ca2+ signaling in rat frontocortical cultured neurons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 07:45:57