Increased synaptic contacts of catecholaminergic boutons in the cerebral cortex and paraventricular hypothalamic nucleus of rats after prenatal and perinatal ethanol exposure.

Prenatal/perinatal exposure to ethanol caused no obvious changes of catecholaminergic terminal density in the cerebral cortex and hypothalamus. However, ethanol induced significant increases of catecholaminergic synaptogenesis in these two regions. Such increased catecholaminergic synaptogenesis may thus be a basis for the etiology of alcohol-induced hyperactive behavior.