| Abstract No.: | B-A2018 |
| Country: | Canada |
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| Title: | THE EFFECTS OF NATURALISTIC PRENATAL ETHANOL EXPOSURE ON THE HIPPOCAMPAL STEM CELL POPULATION IN THE NON-HUMAN PRIMATE |
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| Authors/Affiliations: | 2 Marc Papia*; 2 Mark Burke; 1 Roberta Palmour; 2 Maurice Ptito; 1 Frank Ervin;
1 McGill University, Montreal, QC, Canada; 2 University of Montreal, Montreal, QC, Canada
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| Content: | Purpose: Exposure to ethanol in utero is recognized as a leading cause of preventable developmental disorder. The continuum of fetal alcohol spectrum disorder (FASD), ranging from craniofacial dysmorphology and mental retardation to the much more common developmental learning and behavioral disorders, is now reaching epidemic proportions. Binge-like rodent model systems have concluded that third trimester equivalent ethanol exposure results in hippocampal neuronal loss restricted to the CA1 field. The current study uses a naturalistic and voluntary consumption approach in the non-human primate (Chlorocebus aethiops sabeus) in order to more closely model prenatal ethanol consumption patterns in humans.
Methods: Beginning at about embryonic day 85 (of 165), socially-housed female vervet monkeys voluntarily drank an average of 3.09 + 0.47 g/kg ethanol/day. The control group received isocaloric sucrose. Six animals (3 ethanol exposed, 3 control) were sacrificed at birth for neuroanatomical examination. We have previously reported significant neuronal loss in the CA1, CA2, and CA3 subfields at birth and early adolescence. The goal of the current study was to examine the effect of alcohol exposure on stem cell population in the hippocampus. Serial sections were taken throughout the hippocampus and immunostained with Ki-67, a progenitor marker. All Ki-67 immunopositive cells were counted with a modified stereological procedure using BioQuant Imaging software.
Results: For both ethanol exposed and control groups, the largest concentration of immunopositive cells were located in the granule layer of the dentate gyrus and subgranular/hilus region. In both of these regions ethanol exposed animals demonstrated a reduced density and overall reduction in Ki-67 positive cells.
Conclusion: These data support recent evidence from binge-like rodent models that prenatal ethanol exposure causes deficits in the stem cell population, which may in turn deleteriously affect neurogenesis and neuroplasticity of the hippocampus. |
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