Drugs used to treat affective disorders exert their effects largely through their actions on various neurotransmitter systems. Neurotransmitters are important regulators of neural development. Thus, even limited periods of drug use/exposure during fetal- or postnatal brain ontogeny, which continues to the end of the second decade, can, potentially, cause enduring, functionally significant changes in neuronal circuitry. The duration and timing of drug treatment are critical in determining long-term effects (Popa et al, 2008), owing to developmental changes in the neural substrates on which the drugs act.

Stress, which is associated with affective disorders, adversely impacts neural development during fetal life and postnatally, and is ameliorated by therapies that improve affect. Thus, potential, adverse, long-term effects of exposing the developing brain to medication must be weighed against the deleterious impact of stress elevation as a result of interrupted pharmacotherapy of pregnant women, or not treating children or adolescents.

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