. Author manuscript; available in PMC: 2010 Apr 1.

Published in final edited form as: Nat Rev Neurosci. 2009 Mar 11;10(4):303–312. doi: 10.1038/nrn2598

Table 1.

Neurodevelopmental consequences of prenatal drug exposure.

Age of exposure	Drug	Neurochemistry involved	Neurodevelopmental consequences	References
Late early to mid gestation (primarily based on animal studies)	Cocaine	DA > NE and 5-HT Blocks monoaminergic transporters and Increases synaptic concentrations of monoamines	Altered neuroanatomical morphology, disrupted cognition, altered cellular signaling	¹⁸-³⁷, ⁴²-⁴⁷, ⁵⁴-⁵⁹, ⁶³-⁶⁵, ²⁰³
Throughout gestation	Alcohol	GABA and NMDA Blocks NMDA receptor activity and increases GABAergic activity	Craniofacial dysmorphologies, decreased birth weight, hyperactivity, cognitive deficits, cortical dysgenesis, cell death, reduced brain volume	¹¹³-¹¹⁵, ¹¹⁸- ¹²⁰, ¹²⁶-¹³²
Throughout gestation	Nicotine	Acetylcholine Activates nAChRs	Decreased birth weight, hyperactivity, cognitive disabilities, emotional disruptions	⁸², ⁸⁶-⁹⁴, ⁹⁶- ⁹⁸, ¹⁰⁰-¹⁰⁵, ¹⁰⁷, ¹⁰⁸
Throughout gestation and early postnatal exposure	Amphetamine/ Methamphetamine	DA > NE and 5-HT Reverses the action of monoaminergic transporters and Increases synaptic concentrations of monoamines	Low birth weight, decreased arousal, deficits in learning, decreased volume of hippocampus and striatum	⁶⁶, ⁶⁷, ⁷⁰-⁷³, ⁷⁶-⁸¹