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https://hdl.handle.net/10316/4829
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. | URI: | https://hdl.handle.net/10316/4829 | DOI: | 10.1016/s0006-2952(01)00584-6 | Rights: | openAccess |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
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