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Title: 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
Authors: Ambrósio, António F. 
Silva, Ana P. 
Malva, João O. 
Soares-da-Silva, Patricio 
Carvalho, Arsélio P. 
Carvalho, Caetana M. 
Keywords: Antiepileptic drugs; Carbamazepine; Oxcarbazepine; Sodium channels; Calcium channels; Glutamate release
Issue Date: 2001
Citation: Biochemical Pharmacology. 61:10 (2001) 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 of endogenous 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 did not 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.
DOI: 10.1016/s0006-2952(01)00584-6
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais

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