Prenatal exposure to drugs: effects on brain development and implications for policy and education

Abstract

The effects of prenatal exposure to drugs on brain development are complex and are modulated by the timing, dose and route of drug exposure. It is difficult to assess these effects in clinical cohorts as these are beset with problems such as multiple exposures and difficulties in documenting use patterns. This can lead to misinterpretation of research findings by the general public, the media and policy makers, who may mistakenly assume that the legal status of a drug correlates with its biological impact on fetal brain development and long-term clinical outcomes. It is important to close the gap between what science tells us about the impact of prenatal drug exposure on the fetus and the mother and what we do programmatically with regard to at-risk populations.

Figure 1. Developmental Events and Ontogeny of Drug Targets

The peak periods of key neurodevelopmental events are depicted. Reference to timing of neurotransmitter system development includes appearance of receptors, transporters and synthetic machinery. Note that some of these neurotransmitter elements may continue to mature through puberty. Gestational age for both human (black font) and mouse (red font) are aligned with the black arrow to define the timeline for these events. Emerging drug targets (receptors, transporters, etc) are depicted along this same timeline in purple. Aff, afferents; CP, cortical plate; CTX, cortex; DA, dopamine; E, embryonic; GE, ganglionic eminence; LC, locus coeruleus; M, months; MZ, marginal zone; P, postnatal; PZ, proliferative zone; SP, sub-plate; VTA, ventral tegmental area; W, weeks; 5-HT, serotonin. Adapted from , .