title: Specificity of prenatal cocaine exposure effects on cortical interneurons is independent from dopamine D1 receptor co-localization.
abstract: Gestational cocaine exposure in a rabbit model leads to a persistent increase in parvalbumin immunoreactive cells and processes, reduces dopamine D1 receptor coupling to Gsalpha by means of improper trafficking of the receptor, changes pyramidal neuron morphology, and disrupts cognitive function. Here, experiments investigated whether changes in parvalbumin neurons were specific, or extended to other subpopulations of interneurons. Additionally, we examined dopamine D1 receptor expression patterns and its overlap with specific interneuron populations in the rabbit prefrontal cortex as a possible correlate for alterations in interneuron development following prenatal cocaine exposure. Analysis of calbindin and calretinin interneuron subtypes revealed that they did not exhibit any differences in cell number or process development. Thus, specific consequences of prenatal cocaine in the rabbit appear to be limited to parvalbumin-positive interneurons. Dopamine D1 receptor expression did not correlate with the selective effects of cocaine exposure, however, as both parvalbumin and calbindin cell types expressed the receptor. The findings suggest that additional, unique properties of parvalbumin neurons contribute to their developmental sensitivity to in utero cocaine exposure.
authors.affiliation: Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. blthomps@usc.edu <blthomps@usc.edu>
authors.forename: Barbara L
authors.initials: BL
authors.lastname: Thompson
authors.forename: Gregg D
authors.initials: GD
authors.lastname: Stanwood
authors.forename: Pat
authors.initials: P
authors.lastname: Levitt
mesh_terms: D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D002118:Calcium / Q000378:metabolism; D003042:Cocaine / Q000633:toxicity*; D019970:Cocaine-Related Disorders / Q000150:complications; D004195:Disease Models, Animal; D018765:Dopamine Uptake Inhibitors / Q000633:toxicity; D005260:Female; D007150:Immunohistochemistry; D007395:Interneurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D009421:Nervous System Malformations / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D017397:Prefrontal Cortex / Q000002:abnormalities / Q000187:drug effects* / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism / Q000503:physiopathology*; D011817:Rabbits; D017447:Receptors, Dopamine D1 / Q000187:drug effects* / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000187:drug effects / Q000378:metabolism
chemical_list: D064032:Calbindin 2; D064026:Calbindins; D018765:Dopamine Uptake Inhibitors; D017447:Receptors, Dopamine D1; D064030:S100 Calcium Binding Protein G; D003042:Cocaine; D002118:Calcium