Dopamine, cocaine and the development of cerebral cortical cytoarchitecture: a review of current concepts.
Exposure of the developing fetus to cocaine produces lasting adverse effects on brain structure and function. Animal models show that cocaine exerts its effects by interfering with monoamine neurotransmitter function and that dopamine is cocaine's principal monoamine target in the fetal brain. This review will examine the role of dopamine receptor signaling in the regulation of normal development of the cerebral cortex, the seat of higher cognitive functions, and discuss whether dopamine receptor signaling mechanisms are the principal mediators of cocaine's deleterious effects on the ontogeny of cerebral cortical cytoarchitecture.
Bhide
Pradeep G
PG
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. Bhide@helix.mgh.harvard.eduailto
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000196:embryology / Q000254:growth & development; D003042:Cocaine / Q000633:toxicity*; D004298:Dopamine / Q000633:toxicity*; D005260:Female; D006801:Humans; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D011954:Receptors, Dopamine / Q000187:drug effects / Q000378:metabolism
D011954:Receptors, Dopamine; D003042:Cocaine; D004298:Dopamine