Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
MECHANISM OF THE DYNORPHIN-INDUCED DUALISTIC EFFECT ON FREE INTRACELLULAR CA2+ CONCENTRATION IN CULTURED RAT SPINAL NEURONS
Autore:
HU WH; ZHANG CH; YANG HF; ZHENG YF; LIU N; SUN XJ; JEN J; JEN MF;
Indirizzi:
THIRD MIL MED ACAD,INST SURG RES CHONGQING 630042 PEOPLES R CHINA CHINESE ACAD MED SCI,INST BASIC MED SCI,DEPT PHARMACOL BEIJING 100005PEOPLES R CHINA SCH BASIC MED BEIJING 100005 PEOPLES R CHINA CHINESE ACAD MED SCI,INST BASIC MED SCI,DEPT PHYSIOL BEIJING 100005 PEOPLES R CHINA
Titolo Testata:
European journal of pharmacology
fascicolo: 2-3, volume: 342, anno: 1998,
pagine: 325 - 332
SICI:
0014-2999(1998)342:2-3<325:MOTDDE>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
OPIOID PEPTIDE DYNORPHIN; NMDA RECEPTOR CHANNELS; EXCITATORY AMINO-ACIDS; TRAUMATIC INJURY; CALCIUM CURRENT; CORD INJURY; INVOLVEMENT; PARALYSIS; BINDING; ANTINOCICEPTION;
Keywords:
DYNORPHIN; CA2+; (NEURON); SPINAL CORD; CELL CULTURE; GLUTAMATE RECEPTOR; (RAT); FURA-2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
W.H. Hu et al., "MECHANISM OF THE DYNORPHIN-INDUCED DUALISTIC EFFECT ON FREE INTRACELLULAR CA2+ CONCENTRATION IN CULTURED RAT SPINAL NEURONS", European journal of pharmacology, 342(2-3), 1998, pp. 325-332

Abstract

In order to study the different mechanisms of dynorphin spinal analgesia and neurotoxicity at low and high doses, the effects of various concentrations of dynorphin A-(1-17) on the free intracellular Ca2+ concentration ([Ca2+](i)) in the cultured rat spinal neurons were studied using single cell microspectrofluorimetry. While dynorphin A-(1-17) 0.1-100 mu M had no significant effect on basal [Ca2+](i), dynorphin A-(1-17) 0.1 and 1 mu M significantly decreased the high KCl-evoked peak [Ca2+](i) by 94% and 83% respectively. Dynorphin A-(1-17) 10 and 100 mu M did not affect the peak [Ca2+](i) following K+ depolarization, butin all these neurons there was a sustained and irreversible rise in [Ca2+](i) following high-K+ challenge. Pretreatment with the specific kappa-opioid receptor antagonist nor-binaltorphimine 10 mu M, but not the competitive NMDA receptor antagonist, DL-2-amino-5-phosphonovalerate (APV) 10 mu M, significantly blocked the inhibitory effect of dynorphin A-(1-17) 0.1 mu M on peak [Ca2+](i). However, APV 10 mu M and nor-binaltorphimine 10 mu M significantly antagonized the sustained rise in [Ca2+](i) induced by a high concentration of dynorphin A-(1-17) 10 mu M. Furthermore, in the presence, and following the addition, of increasing concentrations of dynorphin A-(1-17) (0.1, 1, 10 and 100 mu M),the high concentrations of dynorphin A-(1-17) failed to produce a sustained rise in peak [Ca2+](i). These results suggested that dynorphin exerted a dualistic modulatory effect on [Ca2+](i) in cultured rat spinal neurons, inducing a sustained and irreversible intracellular Ca2+ overload via activation of both NMDA and kappa-opioid receptors at higher concentrations, but inhibiting depolarization-evoked Ca2+ influx via kappa-opioid but not NMDA receptors at lower concentrations. Serialaddition of graded concentrations of dynorphin A-(1-17) prevented theeffect of high concentrations of dynorphin A-(1-17) on [Ca2+](i). (C)1998 Elsevier Science B.V.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 18:47:46