Prenatal cocaine decreases the trophic factor S-100β and induced microcephaly

Reversal by postnatal 5-HT1A receptor agonist

Homayoon M. Akbari, Patricia M. Whitaker-Azmitia, Efrain 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 languageEnglish (US)
Pages (from-to)141-144
Number of pages4
JournalNeuroscience Letters
Volume170
Issue number1
DOIs
StatePublished - Mar 28 1994

Fingerprint

Serotonin 5-HT1 Receptor Agonists
Microcephaly
Receptor, Serotonin, 5-HT1A
Cocaine
Neuroglia
Astrocytes
Hippocampus
Parturition
Growth

Keywords

  • Astrocyte
  • Cocaine
  • Ipsapirone
  • Microcephaly
  • Neurodevelopment
  • S-100
  • Serotonin

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Prenatal cocaine decreases the trophic factor S-100β and induced microcephaly : Reversal by postnatal 5-HT1A receptor agonist. / Akbari, Homayoon M.; Whitaker-Azmitia, Patricia M.; Azmitia, Efrain C.

In: Neuroscience Letters, Vol. 170, No. 1, 28.03.1994, p. 141-144.

Research output: Contribution to journalArticle

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