The use of antipsychotic drugs in children has greatly expanded over the past 30 years. This increase occurred despite a lack of research addressing how these drugs affect brain development. This review summarizes and synthesizes preclinical studies that have ascertained the short- and long-term consequences of prenatal and early postnatal antipsychotic drug administration. Antipsychotic drugs are well-known for their ability to block D2-type dopamine receptors and this action features in two main themes that emerge from the literature. First, prenatal antipsychotic drug exposure generally leads to a long-term hypodopaminergic state while early postnatal antipsychotic drug exposure produces a hyperdopaminergic one. Second, the effects of postnatal antipsychotic drug exposure appear roughly similar regardless of age, but drug administration any time prior to puberty (pre or early postnatal) leaves a lasting imprint on neural and behavioral function that persists long after treatment cessation. The enduring brain and behavioral changes seen after early-life antipsychotic administration in animal models provide support for initiatives aimed at reducing the number of children treated with antipsychotics and limiting the dose and length of treatment for those that need them.