PRENATAL COCAINE DECREASES THE TROPHIC FACTOR S-100-BETA AND INDUCED MICROCEPHALY - REVERSAL BY POSTNATAL 5-HT1A RECEPTOR AGONIST

被引：75

作者：

AKBARI, HM

WHITAKERAZMITIA, PM

AZMITIA, EC

机构：

[1] NYU, DEPT BIOL, NEW YORK, NY 10003 USA

[2] SUNY STONY BROOK, DEPT PSYCHIAT, STONY BROOK, NY 11794 USA

来源：

NEUROSCIENCE LETTERS | 1994年 / 170卷 / 01期

关键词：

COCAINE; IPSAPIRONE; NEURODEVELOPMENT; MICROCEPHALY; S-100; ASTROCYTE; SEROTONIN;

D O I：

10.1016/0304-3940(94)90259-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

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页码：141 / 144

页数：4

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