Convulsant actions of calycanthine

Mary Chebib, Rujee K. Duke*, Colin C. Duke, Mark Connor, Kenneth N. Mewett, Graham A R Johnston

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


The principal alkaloid of the family Calycanthaceae, calycanthine has long been recognized as a central convulsant. The alkaloid inhibited the potassium-stimulated release of [3H]GABA from slices of rat hippocampus with an ED50 of ∼21 μM. This effect appeared to be moderately selective since calycanthine at 100 μM had only a weak effect on the potassium-stimulated release of [3H]acetylcholine (15%) and no significant effects on the release of [3H]D-aspartate from hippocampal and cerebellar slices or the release of [3H]glycine from spinal cord slices. Calycanthine blocked the L-type calcium currents with an IC50 of ∼42 μM and also weakly inhibited the N-type calcium currents (IC50 > 100 μM) from neuroblastoma X glioma cells, suggesting voltage-dependent calcium channel blockade as a possible mechanism for its inhibition of GABA and ACh release. Calycanthine was also found to directly inhibit GABA-mediated currents (KB ∼135 μM) from human α1β2γ2L GABAA receptors expressed in Xenopus laevis oocytes but had no effect at 100 μM on human ρ1 GABAc receptors. The results indicated that calycanthine may mediate its convulsant action predominantly by inhibiting the release of the inhibitory neurotransmitter GABA as a result of interactions with L-type Ca2+ channels and by inhibiting GABA-mediated chloride currents at GABAA receptors.

Original languageEnglish
Pages (from-to)58-64
Number of pages7
JournalToxicology and Applied Pharmacology
Issue number1
Publication statusPublished - 1 Jul 2003
Externally publishedYes


  • ACh release
  • Calcium channels
  • Calycanthine
  • Chloride channels
  • GABA release
  • GABA receptor


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