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  • Title: Convulsant actions of calycanthine.
    Author: Chebib M, Duke RK, Duke CC, Connor M, Mewett KN, Johnston GA.
    Journal: Toxicol Appl Pharmacol; 2003 Jul 01; 190(1):58-64. PubMed ID: 12831783.
    Abstract:
    The principal alkaloid of the family Calycanthaceae, calycanthine has long been recognized as a central convulsant. The alkaloid inhibited the potassium-stimulated release of [(3)H]GABA from slices of rat hippocampus with an ED(50) of approximately 21 microM. This effect appeared to be moderately selective since calycanthine at 100 microM had only a weak effect on the potassium-stimulated release of [(3)H]acetylcholine (15%) and no significant effects on the release of [(3)H]D-aspartate from hippocampal and cerebellar slices or the release of [(3)H]glycine from spinal cord slices. Calycanthine blocked the L-type calcium currents with an IC(50) of approximately 42 microM and also weakly inhibited the N-type calcium currents (IC(50) > 100 microM) 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 (K(B) approximately 135 microM) from human alpha(1)beta(2)gamma(2L) GABA(A) receptors expressed in Xenopus laevis oocytes but had no effect at 100 microM on human rho(1) GABA(c) 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 Ca(2+) channels and by inhibiting GABA-mediated chloride currents at GABA(A) receptors.
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