Lamotrigine inhibits Ca2+ currents in cortical neurons: Functional implications

Alessandro Stefani, Francesca Spadoni, Antonio Siniscalchi, Giorgio Bernardi

Research output: Contribution to journalArticle


In pyramidal cortical cells, high-voltage-activated Ca2+ 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 Ca2+ currents (IC50 = 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 Ca2+ channel blocker, ω-conotoxin GVIA (1-3 μM) and the P-type Ca2+ channel blocker, ω-agatoxin-IVA (20-100 nM). These findings demonstrate that lamotrigine, at therapeutic doses, is capable of modulating the Ca2+ 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.

Original languageEnglish
Pages (from-to)113-116
Number of pages4
JournalEuropean Journal of Pharmacology
Issue number1
Publication statusPublished - Jun 20 1996



  • Anti-epileptic drug
  • Ca current
  • Cortex
  • Neuroprotective agent

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

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