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In vivo study: Developmental alterations in primary rat neuronal and glial cell cultures following prenatal cocaine exposure
Author(s) -
Johnson Marquita L,
Womble Tracey,
Jackson Tanise,
Goodman Carl B
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.659.8
Subject(s) - offspring , biology , neuroscience , fetus , in vivo , neuroglia , prenatal cocaine exposure , central nervous system , pregnancy , prenatal exposure , genetics
Evidence has shown that prenatal cocaine exposure to the developing fetus is associated with neurological and behavioral abnormalities. These alterations are attributed to structural damage in the brain as well as neurodevelopment with no significant underlying mechanisms. Since the effects of prenatal cocaine exposure on glial and neuronal development are largely unclear, there is a need to establish an appropriate animal model to evaluate cocaine's antecedent role in the occurrence of neuronal and glial cell maturation. The present study addresses the hypothesis that chronic prenatal cocaine exposure alters the maturation and function of neurons and glial cells in the offspring. Timed pregnant Sprague‐Dawley rats were treated with 40 mg/kg of cocaine on gestational day 10–21. The brain tissue of the pups was harvested to yield pure neuronal and glial cell cultures. ICC analysis confirmed the successful isolation of primary neurons and glial cells, as well as morphological differences between the control and treatment pups among these cell types. Western Blot analysis determined a variation of protein expression. A cytokine array was used to identify cytokine expression levels. These studies suggest that cocaine alters growth, maturation, and function of growing neuronal and glial cell cultures. Excessive glial cell activation can cause harm to neurons in regards to their development and plasticity.