Cocaine exposure decreases GABA neuron migration from the ganglionic eminence to the cerebral cortex in embryonic mice
UMass Chan Affiliations
E.K. Shriver Center for Mental RetardationDocument Type
Journal ArticlePublication Date
2004-04-01Keywords
AnimalsCell Movement
Cerebral Cortex
Cocaine
Dose-Response Relationship, Drug
Median Eminence
Mice
Neurons
Olfactory Bulb
gamma-Aminobutyric Acid
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
Recurrent exposure of the developing fetus to cocaine produces persistent alterations in structure and function of the cerebral cortex. Neurons of the cerebral cortex are derived from two sources: projection neurons from the neuroepithelium of the dorsal pallium and interneurons from the ganglionic eminence of the basal telencephalon. The interneurons are GABAergic and reach the cerebral cortex via a tangential migratory pathway. We found that recurrent, transplacental exposure of mouse embryos to cocaine from embryonic day 8 to 15 decreases tangential neuronal migration and results in deficits in GABAergic neuronal populations in the embryonic cerebral wall. GABAergic neurons of the olfactory bulb, which are derived from the ganglionic eminence via the rostral migratory pathway, are not affected by the cocaine exposure suggesting a degree of specificity in the effects of cocaine on neuronal migration. Thus, one mechanism by which prenatal cocaine exposure exerts deleterious effects on cerebral cortical development may be by decreasing GABAergic neuronal migration from the ganglionic eminence to the cerebral wall. The decreased GABA neuron migration may contribute to persistent structural and functional deficits observed in the exposed offspring.Source
Cereb Cortex. 2004 Jun;14(6):665-75. Epub 2004 Mar 28. Link to article on publisher's site
DOI
10.1093/cercor/bhh027Permanent Link to this Item
http://hdl.handle.net/20.500.14038/41161PubMed ID
15054047Related Resources
ae974a485f413a2113503eed53cd6c53
10.1093/cercor/bhh027