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Dendritic morphology is altered in hippocampal neurons following prenatal compromise
1Department of Anatomy and Cell Biology, University of Melbourne, Parkville, 3010, Victoria, Australia. s.dieni@anatomy.edu.au
Insights
Chronic placental insufficiency (CPI) in guinea pigs caused significant changes in fetal brain development, specifically altering hippocampal neuron dendrites. These structural brain alterations may contribute to neurological deficits after birth.
Area of Science:
- Neuroscience
- Developmental Biology
- Obstetrics
Background:
- Chronic placental insufficiency (CPI) is a known cause of intrauterine growth restriction (IUGR).
- Previous studies showed reduced hippocampal neuropil volumes in growth-restricted (GR) fetal brains.
- Understanding specific cellular changes is crucial for predicting postnatal neurological deficits.
Purpose of the Study:
- To investigate the specific effects of experimentally induced CPI on the dendritic morphology of hippocampal neurons in fetal guinea pigs.
- To determine if growth restriction impacts dendritic elongation, branching, and spine density in CA1 pyramidal neurons and dentate granule cells.
Main Methods:
- CPI was induced in pregnant guinea pigs via unilateral uterine artery ligation.
- Hippocampi from control and GR fetuses were analyzed using the Rapid Golgi technique.
- Dendritic morphology was quantified using the Sholl method, and dendritic spine density was measured.
Main Results:
- Growth-restricted (GR) fetal brains showed reduced dendritic elongation and altered branching in CA1 pyramidal neurons.
- Dentate granule cells in GR brains exhibited reduced dendritic outgrowth.
- Increased dendritic spine density was observed in both neuronal populations in GR brains, potentially due to altered pruning or compensation.
Conclusions:
- Experimentally induced chronic placental insufficiency leads to selective alterations in hippocampal neuron dendritic morphology in fetal guinea pigs.
- These prenatal structural brain changes may underlie functional deficits observed in the postnatal period.
- Findings highlight the vulnerability of fetal brain development to placental insufficiency.
Abstract:
Chronic placental insufficiency (CPI), a known cause of intrauterine growth restriction, can lead to structural alterations in the developing brain that might underlie postnatal neurological deficits. We have previously demonstrated significant reductions in the volumes of hippocampal neuropil layers in fetal guinea pig brains following experimentally induced growth restriction. To determine the components of the neuropil affected in the brains of growth restricted (GR) fetuses, the dendritic morphology of CA1 pyramidal neurons and dentate granule cells was examined. CPI was induced by unilateral uterine artery ligation in pregnant guinea pigs at midgestation (term approximately 67 days). Hippocampi from control and GR fetuses were stained using the Rapid Golgi technique and the growth and branching of the dendritic arbors were quantified using the Sholl method. In addition, the density of dendritic spines was determined on the apical arbors of each population. In GR brains (n = 7) compared to controls (n = 7), there was a reduction in dendritic elongation (p < 0.005) and an alteration in the branch point distribution in CA1 basal arbors, and a reduction both in the outgrowth (p < 0.05) and branch point number (p < 0.05) of CA1 apical arbors. Dentate granule cells from GR brains also demonstrated reduced dendritic outgrowth (p < 0.05). There was an increase in dendritic spine density in both neuronal populations; this might be due either to altered synaptic pruning or as a compensatory mechanism for reduced dendritic length. These findings demonstrate that a chronic prenatal insult causes selective changes in the morphology of hippocampal cell dendrites and may lead to alterations in hippocampal function in the postnatal period.