Paralysis and skeletal abnormalities in chick embyos treated with Physostigmine

Abstract

In the chick embryo, physostigmine causes micromelia, wry neck and parrot beak. It has been known for some years that nicotinamide prevents the beak and limb defects, but not the neck anomaly. Since the latter also occurs in embryos paralysed with decamethonium, the present study investigates the role of paralysis of muscle in the development of this anomaly in physostigmine-treated embryos. When sufficient nicotinamide to prevent micromelia and parrot beak is supplied, a syndrome of bony anomalies indistinguishable from that in decamethonium-paralysed embryos is observed. Direct observations of treated embryos in ovo show that physostigmine causes prolonged muscle paralysis. It is concluded that physostigmine exerts teratogenic effects in the chick embryo by two separate mechanisms of action: parrot beak and micromelia are presumably due to interference with the metabolism of nicotinamide; wry neck and certain other malformations are consequences of paralysis resulting from cholinesterase inhibition at motor end plates in skeletal muscle.