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Titolo:
Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists
Autore:
Ambrosio, AF; Silva, AP; Malva, JO; Soares-da-Silva, P; Carvalho, AP; Carvalho, CM;
Indirizzi:
Univ Coimbra, Ctr Neurosci Coimbra, Dept Cell Biol, P-3004517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3004517 iol, P-3004517 Coimbra, Portugal Univ Coimbra, Fac Med, Biochem Lab, P-3004517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3004517 Lab, P-3004517 Coimbra, Portugal BIAL, S Mamede Coronado, Portugal BIAL S Mamede Coronado PortugalBIAL, S Mamede Coronado, Portugal
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 9, volume: 38, anno: 1999,
pagine: 1349 - 1359
SICI:
0028-3908(199909)38:9<1349:CILCCI>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBELLAR GRANULE CELLS; TEMPORAL-LOBE EPILEPSY; KAINIC ACID; IN-VITRO; EXTRACELLULAR SEROTONIN; ANTICONVULSANT ACTION; ANTIEPILEPTIC DRUG; CALCIUM CURRENTS; KINDLING MODEL; PHENYTOIN;
Keywords:
carbamazepine; glutamate ionotropic receptors; kainate; voltage-sensitive Ca2+ channels; voltage-sensitive Na+ channels; [Ca2+](i); [Na+](i);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Carvalho, CM Univ Coimbra, Ctr Neurosci Coimbra, Dept Cell Biol, P-3004517Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3004517 7 Coimbra, Portugal
Citazione:
A.F. Ambrosio et al., "Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists", NEUROPHARM, 38(9), 1999, pp. 1349-1359

Abstract

In order to better understand the mechanism(s) of action of carbamazepine (CBZ), we studied its effects on the increase in [Ca2+](i) and [Na+](i) stimulated by glutamate ionotropic receptor agonists, in cultured rat hippocampal neurons, as followed by indo-1 or SBFI fluorescence, respectively. CBZ inhibited the increase in [Ca2+](i) stimulated either by glutamate, kainate, alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA), or N-methyl-D-aspartate (NMDA), in a concentration-dependent manner. In order to discriminate the effects of CBZ on the activation of glutamate receptors from possible effects on Ca2+ channels, we determined the inhibitory effects of Ca2+ channel blockers on [Ca2+](i) changes in the absence or in the presence of CBZ. The presence of 1 mu M nitrendipine, 0.5 mu M omega-conotoxin GVIA (omega-CgTx GVIA), or of both blockers, inhibited the kainate-stimulated increase in [Ca2+](i) by 51.6, 32.9 or 68.7%, respectively. In the presence of both 100 mu M CBZ and nitrendipine, the inhibition was similar (54.1%) tothat obtained with nitrendipine alone, but in the presence of both CBZ andomega-CgTx GVIA, the inhibition was greater (54%) than that caused by omega-CgTx GVIA alone. However, CBZ did not inhibit the increase in [Na+](i) stimulated by the glutamate receptor agonists, but inhibited the increase in [Na+](i) due to veratridine. Tetrodotoxin, or MK-801, did not inhibit the influx of Na+ stimulated by kainate, indicating that Na+ influx occurs mainly through the glutamate ionotropic non-NMDA receptors. Moreover, LY 303070,a specific AMPA receptor antagonist, inhibited the [Na+](i) response to kainate or AMPA by about 70 or 80%, respectively, suggesting that AMPA receptors are mainly involved. Taken together, the results suggest that CBZ inhibits L-type Ca2+ channels and Na+ channels, but does not inhibit activation of glutamate ionotropic receptors. (C) 1999 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 15:52:25