PT  - JOURNAL ARTICLE
AU  - M Alkondon
AU  - E F Pereira
AU  - S Wonnacott
AU  - E X Albuquerque
TI  - Blockade of nicotinic currents in hippocampal neurons defines methyllycaconitine as a potent and specific receptor antagonist.
DP  - 1992 Apr 01
TA  - Molecular Pharmacology
PG  - 802--808
VI  - 41
IP  - 4
4099  - http://molpharm.aspetjournals.org/content/41/4/802.short
4100  - http://molpharm.aspetjournals.org/content/41/4/802.full
SO  - Mol Pharmacol1992 Apr 01; 41
AB  - Methyllycaconitine, a toxin isolated from the seeds of Delphinium brownii, inhibited acetylcholine- and anatoxin-induced whole-cell currents in cultured fetal rat hippocampal neurons, at picomolar concentrations. This antagonism was specific, concentration dependent, reversible, and voltage independent. Furthermore, methyllycaconitine inhibited 125I-alpha-bungarotoxin binding to adult rat hippocampal membranes, protected against the alpha-bungarotoxin-induced pseudoirreversible blockade of nicotinic currents, and shifted the concentration-response curve of acetylcholine to the right in fetal rat hippocampal neurons, suggesting a possible competitive mode of action for this toxin. Remarkably low concentrations of methyllycaconitine (1-1000 fM) decreased the frequency of anatoxin-induced single-channel openings, with no detectable decrease in the mean channel open time. These actions of methyllycaconitine commend this neurotoxin for the characterization of the alpha-bungarotoxin-sensitive subclass of neuronal nicotinic receptors, which has hitherto eluded functional demonstration.