Abstract
In pyramidal cortical cells, high-voltage-activated Ca 2− currents affect seizure propagation and the release of excitatory amino acids at the corticostriatal axon terminals. The new antiepileptic drug lamotrigine (Lamictal) produced a large and dose-dependent inhibition of high-voltage-activated Ca 2+ currents (IC 50 = 12.3 μM) in rat cortical neurons. This action was not blocked by the dihydropyridine receptor antagonist nifedipine; instead, the response was blocked by the concomitant application of the N-type Ca 2+ channel blocker, ω-conotoxin GVIA (1–3 μM) and the P-type Ca 2+ channel blocker, ω-agatoxin-IVA (20–100 nM). These findings demonstrate that lamotrigine, at therapeutic doses, is capable of modulating the Ca 2+ conductances involved in excitatory amino acid release in the corticostriatal pathway, partially explaining lamotrigine usefulness in the therapy of epilepsy as well as in the treatment of excitatory amino acid-induced neurotoxicity.
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