Neuropharmacologic teratogenesis and neurotransmitter regulation of palate development

Neuropharmacologic agents may be more teratogenic to human beings by perturbing neurotransmitter mechanisms that regulate embryonic development. There is evidence that neurotransmitters function in mouse palate development: Serotonin and acetylcholine stimulate and GABA inhibits shelf reorientation. Both serotonin and GABA have been measured in the palate and uptake systems monitored. Serotonin stimulates cell motility, protein carboxyl methylation, and cyclic GMP. Diazepam (Valium) could cause cleft palate by mimicking GABA. Genetic differences in both diazepam teratogenesis and in a GABAergic system of the mouse have been observed. If human beings were to show genetic differences in a GABAergic system, some pregnant women could be at high risk when treated with diazepam.