Abstract
In utero exposure to cocaine results in neurobehavioral abnormalities in both clinical and laboratory studies. Cocaine administration from embryonic day 13 to parturition disrupts the distribution of S-100-positive astrocytes in the hippocampus and subplate region of the cortex in cocaine-exposed animals. Postnatal treatment with ipsapirone, a 5-HT1A agonist, shown to stimulate glial release of S-100, alleviated the cellular disruptions and growth retardation caused by prenatal cocaine exposure.
MeSH terms
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Animals
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Astrocytes / drug effects
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Astrocytes / metabolism
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism
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Cocaine / antagonists & inhibitors*
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Cocaine / toxicity
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Female
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Hippocampus / cytology
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Hippocampus / drug effects
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Hippocampus / metabolism
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Immunohistochemistry
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Microcephaly / chemically induced
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Microcephaly / prevention & control*
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Pregnancy
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Prenatal Exposure Delayed Effects
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Pyrimidines / pharmacology
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Rats
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Rats, Sprague-Dawley
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S100 Proteins / immunology
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S100 Proteins / metabolism*
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Serotonin Antagonists / pharmacology
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Serotonin Receptor Agonists / pharmacology*
Substances
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Pyrimidines
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S100 Proteins
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Serotonin Antagonists
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Serotonin Receptor Agonists
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ipsapirone
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Cocaine