Effects of in utero ethanol exposure and maternal treatment with a 5-HT(1A) agonist on S100B-containing glial cells

• Published in: Brain research. Developmental brain research 2000-06, Vol.121 (2), p.133
• Main Authors: Eriksen, J L, Gillespie, R A, Druse, M J
• Format: Article
• Language: English
• Subjects: Animals; Buspirone - pharmacology; Calcium-Binding Proteins - analysis; Calcium-Binding Proteins - genetics; Cell Count - drug effects; Central Nervous System Depressants - pharmacology; Ethanol - pharmacology; Female; Fetal Alcohol Spectrum Disorders - drug therapy; Fetal Alcohol Spectrum Disorders - prevention & control; Gene Expression - drug effects; In Situ Hybridization; Nerve Growth Factors - analysis; Nerve Growth Factors - genetics; Neuroglia - chemistry; Neuroglia - drug effects; Pregnancy; Prenatal Exposure Delayed Effects; Pyrimidines - pharmacology; Raphe Nuclei - abnormalities; Raphe Nuclei - chemistry; Raphe Nuclei - drug effects; Rats; Rats, Sprague-Dawley; Receptors, Serotonin - physiology; Receptors, Serotonin, 5-HT1; RNA, Messenger - analysis; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Serotonin Receptor Agonists - pharmacology
• ISSN: 0165-3806
• DOI: 10.1016/S0165-3806(00)00029-8

This laboratory previously showed that in utero ethanol exposure severely impairs the development of the cell bodies and projections of serotonin (5-HT) neurons, and that maternal treatment with a 5-HT(1A) agonist prevents many of these abnormalities. Others demonstrated that stimulation of fetal astroglial 5-HT(1A) receptors increases production and release of S100B, a glial trophic factor that is essential for the development of 5-HT neurons. The present study investigated a potential mechanism by which ethanol hinders development of 5-HT neurons, and by which maternal 5-HT(1A) agonist treatment prevents this damage. This study tested the hypothesis that in utero ethanol exposure reduces the number of S100B immunopositive glia and that maternal 5-HT(1A) agonist treatment prevents ethanol-associated changes in S100B. To test our hypothesis, we determined the effects of in utero ethanol exposure and maternal treatments with the 5-HT(1A) agonists ipsapirone and buspirone on S100B immunopositive glial cells. On gestation day 20 (G20), S100B immunopositive cells were quantified in the midline raphe glial structure (MRGS), a large transient structure that contains substantial numbers of S100B-positive glial cells and that spans the dorsal raphe, median raphe, and B9 complex of 5-HT neurons. S100B immunopositive glial cells were also determined in an area proximal to the dorsal raphe in postnatal day 2 (PN2) rats. In utero ethanol exposure significantly reduced S100B immunopositive glial cells in the MRGS at G20 and in the dorsal raphe at PN2. In addition, treatment of pregnant rats with a 5-HT(1A) agonist between G13 and G20 prevented the ethanol-associated reduction in S100B immunopositive glial cells. These studies demonstrated that part of ethanol's damaging effects on developing 5-HT neurons is mediated by a reduction of S100B and that some of the protective effects of maternal 5-HT(1A) agonist treatment are related to the actions of these drugs on glial cells.