Prenatal cocaine decreases the trophic factor S-100 beta and induced microcephaly: reversal by postnatal 5-HT1A receptor agonist

H. M. Akbari, P. M. Whitaker-Azmitia, E. C. Azmitia

Research output: Contribution to journalArticle

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.
Original languageUndefined
Pages (from-to)141-4
JournalNeuroscience Letters
Volume170
Issue number1
StatePublished - 1994

Keywords

  • Animals Astrocytes/drug effects/metabolism Cerebral Cortex/cytology/drug effects/metabolism Cocaine/*antagonists & inhibitors/toxicity Female Hippocampus/cytology/drug effects/metabolism Immunohistochemistry Microcephaly/chemically induced/*prevention & control Pregnancy Prenatal Exposure Delayed Effects Pyrimidines/pharmacology Rats Rats, Sprague-Dawley S100 Proteins/immunology/*metabolism Serotonin Antagonists/pharmacology Serotonin Receptor Agonists/*pharmacology

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