Astroglial Plasticity Is Implicated in Hippocampal Remodelling in Adult Rats Exposed to Antenatal Dexamethasone
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Published on: March 31, 2015
Vishvesh H Shende1, Simon McArthur2, Glenda E Gillies3
1Department of Life Sciences, University of Roehampton, London SW15 4JD, UK.
Insights
Antenatal dexamethasone exposure in rats reduced hippocampus size and impaired glial cell structure, indicating potential long-term brain development issues. This prenatal treatment led to maladaptive glial plasticity in the hippocampus.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Prenatal exposure to corticosteroids like dexamethasone is common for fetal lung maturation.
- Long-term effects on brain development, particularly neuroplasticity, require further investigation.
Purpose of the Study:
- To investigate the long-term effects of maternal dexamethasone treatment on brain structure and glial morphology in male rat offspring.
- To assess the impact on the hippocampus, amygdala, and nucleus accumbens.
Main Methods:
- Stereological analysis of brain regions (dorsal hippocampus, basolateral amygdala, nucleus accumbens) in 3-month-old Sprague Dawley rats.
- Micro-computed tomography (micro-CT) for total brain volume assessment.
- GFAP-immunoreactive astroglial cell morphology and cell number quantification.
Main Results:
- Dexamethasone treatment did not affect total brain volume or cell numbers in the studied regions.
- A significant 8% reduction in the relative dorsal hippocampus volume was observed.
- Significant reductions in total and mean primary process length of hippocampal astrocytes (CA1, CA3, DG) were noted, indicating altered glial morphology.
Conclusions:
- Prenatal dexamethasone exposure leads to a reduction in hippocampal volume and significant alterations in hippocampal astroglial morphology.
- These changes suggest a form of maladaptive glial plasticity induced by prenatal dexamethasone exposure.
- The basolateral amygdala and nucleus accumbens showed no significant changes in volume or glial morphology.
Abstract:
The long-term effects of antenatal dexamethasone treatment on brain remodelling in 3-month-old male Sprague Dawley rats whose mothers had been treated with dexamethasone were investigated in the present study. Dorsal hippocampus, basolateral amygdala and nucleus accumbens volume, cell numbers, and GFAP-immunoreactive astroglial cell morphology were analysed using stereology. Total brain volume as assessed by micro-CT was not affected by the treatment. The relative volume of the dorsal hippocampus (% of total brain volume) showed a moderate, by 8%, but significant reduction in dexamethasone-treated versus control animals. Dexamethasone had no effect on the total and GFAP-positive cell numbers in the hippocampal subregions, basolateral amygdala, and nucleus accumbens. Morphological analysis indicated that numbers of astroglial primary processes were not affected in any of the hippocampal subregions analysed but significant reductions in the total primary process length were observed in CA1 by 32%, CA3 by 50%, and DG by 25%. Mean primary process length values were also significantly decreased in CA1 by 25%, CA3 by 45%, and DG by 25%. No significant astroglial morphological changes were found in basolateral amygdala and nucleus accumbens. We propose that the dexamethasone-dependent impoverishment of hippocampal astroglial morphology is the case of maladaptive glial plasticity induced prenatally.
