In utero exposure to cocaine delays postnatal synaptic maturation of glutamatergic transmission in the VTA

Cocaine can easily cross the placental and fetal blood-brain barrier, and in utero exposure to cocaine can cause lasting behavioral changes in postnatal periods. Here, Bellone et al. studied the physiological and circuit level mechanism behind the consequence of in utero cocaine exposure and found a postnatal synaptic maturation defect of excitatory input to the dopaminergic neurons in the ventral tegmental area of mice. In particular, they found that late embryonic in utero cocaine exposure causes a delay in AMPAR/NMDAR switch in early postnatal mouse brain.