early and widespread influence of serotonergic, dopaminergic and glutamatergic systems on neuronal growth and connectivity provides a strong theoretical basis for suspecting that prenatal exposure to METH and other neurotoxic amphetamines may also result in alterations in developing neural circuitry53. In a fetal rat model of low and high-dose gestational METH exposure, Weissman and Caldecott-Hazard produced both serotonergic neurotoxic effects and synaptic remodeling of axonal terminals55. More recently, Jeng et al. identified oxidative DNA damage in the brains of embryonic and fetal mice, along with resultant postnatal motor deficits, after exposure to a single dose of METH56.
