Lamotrigine and carbamazepine affect differently the release of D-[3H]aspartate from mouse cerebral cortex slices : Involvement of NO

The effects of lamotrigine and carbamazepine on the release of preloaded D-[3H]aspartate and the involvement of nitric oxide were studied with mouse cerebral cortical slices in a superfusion system. Lamotrigine inhibited the veratridine-evoked release, whereas the K+-stimulated release was attenuate...

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Bibliographic Details
Published in:Neurochemical research 1999-09, Vol.24 (9), p.1153-1159
Main Authors: AFANAS'EV, I, KUDRIN, V, RAYEVSKY, K. S, VARGA, V, SARANSAARI, P, OJA, S. S
Format: Article
Language:English
Subjects:
2-Amino-5-phosphonovalerate - pharmacology
Animals
aspartic acid
Aspartic Acid - metabolism
carbamazepine
Carbamazepine - pharmacology
Cerebral Cortex - drug effects
Cerebral Cortex - metabolism
Enzyme Inhibitors - pharmacology
In Vitro Techniques
Lamotrigine
Male
Mice
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitric Oxide Synthase - antagonists & inhibitors
Nitroarginine - pharmacology
Triazines - pharmacology
Tritium
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Summary:The effects of lamotrigine and carbamazepine on the release of preloaded D-[3H]aspartate and the involvement of nitric oxide were studied with mouse cerebral cortical slices in a superfusion system. Lamotrigine inhibited the veratridine-evoked release, whereas the K+-stimulated release was attenuated more strongly by carbamazepine than by lamotrigine. These effects were accentuated by the N-methyl-D-aspartate receptor antagonist L-2-amino-5-phosphonovalerate and the nitric oxide synthase inhibitor L-nitroarginine, but diminished by the nitric oxide donor sodium nitroprusside. The results show that in addition to the blockade of voltage-sensitive Na+ (and Ca2+) channels, NO-mediated mechanisms are probably involved in the anticonvulsant actions of carbamazepine and, in particular, those of lamotrigine.
ISSN:0364-3190
1573-6903
DOI:10.1023/A:1020716621300