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.
|State||Published - 1994|
- 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
Akbari, H. M., Whitaker-Azmitia, P. M., & Azmitia, E. C. (1994). Prenatal cocaine decreases the trophic factor S-100 beta and induced microcephaly: reversal by postnatal 5-HT1A receptor agonist. Neuroscience Letters, 170(1), 141-4.