Abstract:
:Remacemide is a potential anticonvulsant drug with an active metabolite, desglycinyl-remacemide (DGR). Both moieties have been reported to block neuronal Na(+) channels and the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. The effects of remacemide and DGR on zero Mg(2+)/4-aminopyridine-induced epileptiform discharges were investigated in the rat hippocampal slice preparation and compared with carbamazepine (CBZ), a prototypic Na(+) channel blocker, and AR-R15896AR, a putative NMDA channel blocker. Remacemide (0-100 microM) was without significant effect, while DGR, CBZ and AR-R15896AR all decreased burst frequency in a concentration (0-100 microM) dependent manner. These findings suggest that remacemide is not sufficiently potent at the Na(+) channel or NMDA receptor to attenuate epileptiform activity in this model and that the anticonvulsant effects of the drug may be mediated by DGR.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Santangeli S,Sills GJ,Stone TW,Brodie MJdoi
10.1016/s0304-3940(01)02511-3keywords:
subject
Has Abstractpub_date
2002-03-15 00:00:00pages
33-6issue
1-2eissn
0304-3940issn
1872-7972pii
S0304394001025113journal_volume
321pub_type
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