Prenatal alcohol exposure and the neuroapoptosis with long-term effect in visual cortex of mice

Alcohol Alcohol. 2007 Jul-Aug;42(4):285-90. doi: 10.1093/alcalc/agm032. Epub 2007 May 30.

Abstract

Aims: The prenatal ethanol exposure induced neuroapoptosis and neuron loss in visual cortex would be investigated in mice at P0, P7 and P14.

Methods: Intubating pregnant mice ethanol daily began on E5 and continued through the pup's birth. The neuroapoptosis in visual cortex was visualized by the caspase 3 immunocytochemistry, and the neuron loss was observed with Nissl method as well.

Results: With prenatal ethanol exposure, the dose-dependent neuroapoptosis and neuron loss in visual cortex could be found at P0 and even at P7 and P14 as well.

Conclusions: The prenatal ethanol exposure induced neuroapoptosis and neuron loss will persist into postnatal stage, and the long-term effect of neuroapoptosis might be one of the causes of postnatal neurobehavioural disturbances associated with fetal alcohol syndrome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Central Nervous System Depressants / blood
  • Central Nervous System Depressants / toxicity*
  • Coloring Agents
  • Dose-Response Relationship, Drug
  • Eosine Yellowish-(YS)
  • Ethanol / blood
  • Ethanol / toxicity*
  • Female
  • Hematoxylin
  • Immunohistochemistry
  • Mice
  • Mice, Inbred C57BL
  • Neurons / drug effects*
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • Visual Cortex / drug effects*

Substances

  • Central Nervous System Depressants
  • Coloring Agents
  • Ethanol
  • Caspase 3
  • Eosine Yellowish-(YS)
  • Hematoxylin