Coniine, an
alkaloid from Conium maculatum (poison hemlock), has been shown to be teratogenic in livestock. The major teratogenic outcome is
arthrogryposis, presumably due to
nicotinic receptor blockade. However,
coniine has failed to produce
arthrogryposis in rats or mice and is only weakly teratogenic in rabbits. The purpose of this study was to evaluate and compare the effects of
coniine and
nicotine in the developing chick. Concentrations of
coniine and
nicotine sulfate were 0.015%, 0.03%, 0.075%, 0.15%, 0.75%, 1.5%, 3%, and 6% and 1%, 5%, and 10%, respectively. Both compounds caused deformations and lethality in a dose-dependent manner. All concentrations of
nicotine sulfate caused some lethality but a no effect level for
coniine lethality was 0.75%. The deformations caused by both
coniine and
nicotine sulfate were excessive flexion or extension of one or more toes. No histopathological alterations or differences in bone formation were seen in the limbs or toes of any chicks from any group; however, extensive cranial
hemorrhage occurred in all
nicotine sulfate-treated chicks. There was a statistically significant (P < or = 0.01) decrease in movement in
coniine and
nicotine sulfate treated chicks as determined by ultrasound. Control chicks were in motion an average of 33.67% of the time, while
coniine-treated chicks were only moving 8.95% of a 5-min interval, and no movement was observed for
nicotine sulfate treated chicks. In summary, the chick embryo provides a reliable and simple experimental animal model of
coniine-induced
arthrogryposis. Data from this model support a mechanism involving
nicotinic receptor blockade with subsequent decreased fetal movement.