Effects of ethanol on glial cell proliferation

Relevance to the Fetal Alcohol Syndrome

Marina Guizzetti, M. Catlin, L. G. Costa

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Exposure to ethanol during pregnancy is detrimental to brain development. Individuals affected by the Fetal Alcohol Syndrome present a number of central nervous system dysfunctions including microencephaly and mental retardation. Studies on the mechanisms of ethanol's developmental neurotoxicity have focused on its interaction with neurons; however, emerging evidence is suggesting that ethanol can significantly affect glial cells as well. A number of in vitro studies have shown that ethanol can inhibit the proliferation of various glial cells (mostly primary astrocytes or astrocytoma cells) at relatively high concentrations (100-200 mM). On the other hand, proliferation induced by some, but not all mitogens, is inhabited by low concentrations (10-50 mM) of ethanol. These inhibitory effects of ethanol may contribute to its developmental neurotoxicity observed following in vivo exposure. Animal models have indeed shown that ethanol causes microencephaly when given during the brain growth spurt, a period of brain development characterized by astroglial proliferation and maturation.

Original languageEnglish (US)
Pages (from-to)433-443
Number of pages11
JournalPediatric Pathology and Molecular Medicine
Volume18
Issue number4-5
StatePublished - 1998
Externally publishedYes

Fingerprint

Fetal Alcohol Spectrum Disorders
Neuroglia
Ethanol
Cell Proliferation
Brain
Astrocytoma
Mitogens
Astrocytes
Intellectual Disability
Central Nervous System
Animal Models
Neurons
Pregnancy
Growth

Keywords

  • Astrocytes
  • Ethanol
  • Fetal Alcohol Syndrome

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Pediatrics, Perinatology, and Child Health

Cite this

Effects of ethanol on glial cell proliferation : Relevance to the Fetal Alcohol Syndrome. / Guizzetti, Marina; Catlin, M.; Costa, L. G.

In: Pediatric Pathology and Molecular Medicine, Vol. 18, No. 4-5, 1998, p. 433-443.

Research output: Contribution to journalArticle

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