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Titolo:
Inhibition of glutamate release by BIA 2-093 and BIA 2-024, two novel derivatives of carbamazepine, due to blockade of sodium but not calcium channels
Autore:
Ambosio, 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 Dept Res & Dev, P-4785 S Mamede Do Coronado, Portugal Dept Res & Dev S Mamede Do Coronado Portugal P-4785 o Coronado, Portugal
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 10, volume: 61, anno: 2001,
pagine: 1271 - 1275
SICI:
0006-2952(20010515)61:10<1271:IOGRBB>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
CA2+ CHANNELS; OXCARBAZEPINE; PHARMACOLOGY; SYNAPTOSOMES; VERATRIDINE; LAMOTRIGINE; PHENYTOIN; RECEPTOR; EPILEPSY;
Keywords:
antiepileptic drugs; carbamazepine; oxcarbazepine; sodium channels; calcium channels; glutamate release;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
14
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. Ambosio et al., "Inhibition of glutamate release by BIA 2-093 and BIA 2-024, two novel derivatives of carbamazepine, due to blockade of sodium but not calcium channels", BIOCH PHARM, 61(10), 2001, pp. 1271-1275

Abstract

We investigated the mechanism(s) of action of two new putative antiepileptic drugs (AEDs), (S)-(-)-10-acetoxy-10,11-dihydro-5H-dibenz[b,f]azepine-5-carboxamide (BIA 2-093) and 10,11-dihydro-10-hydroxyimino-5H-dibenz[b,f]azepine-5-carboxamide (BIA 2-024). by comparing their effects on the release ofendogenous glutamate in hippocampal synaptosomes. with those of carbamazepine (CBZ) and oxcarbazepine (OXC). The AEDs inhibited the release of glutamate evoked by 4-aminopyridine (4-AP) or veratridine in a concentration-dependent manner, being CBZ more potent than the other AEDs. Using conditions of stimulation (30 mM KCl), where Na+ channels are inactivated, the AEDs didnot inhibit either the Ca2+-dependent or -independent release of glutamate. The results indicate that BIA 2-093 and BIA 2-024 have sodium channel-blocking properties, but CBZ and OXC are more potent than the new AEDs. Moreover, the present data also indicate that Ca2+ channels coupled to the exocytotic release of glutamate and the activity of the glutamate transporter were not affected by the AEDs. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 09:52:42