Effects of neonatal corticosteroid treatment on hippocampal synaptic function
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Updated: Jul 13, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Chiung-Chun Huang1, Hsiue-Ru Lin, Ying-Ching Liang
1Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City 701, Taiwan.
Insights
Neonatal dexamethasone (DEX) treatment for chronic lung disease (CLD) impairs long-term memory and synaptic plasticity in adolescent rats. Hydrocortisone (HC) did not show these adverse neurodevelopmental effects, suggesting it may be a safer alternative.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Neonatal corticosteroid treatment is used for chronic lung disease (CLD).
- Concerns exist regarding long-term neurodevelopmental outcomes in infants treated with corticosteroids.
- Dexamethasone (DEX) and hydrocortisone (HC) are commonly used corticosteroids.
Purpose of the Study:
- To investigate the long-term effects of neonatal dexamethasone (DEX) and hydrocortisone (HC) treatment on hippocampal synaptic plasticity and associative memory.
- To compare the neurodevelopmental consequences of DEX versus HC in later life.
Main Methods:
- Neonatal rats received tapering doses of DEX or HC.
- Electrophysiological recordings assessed long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus.
- Biochemical assays measured Ca2+/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and protein phosphatase 1 (PP1) expression.
- Passive avoidance learning tasks evaluated memory retention.
Main Results:
- Neonatal DEX treatment, but not HC, impaired LTP and enhanced LTD induction in adolescent rats.
- DEX-induced changes in synaptic plasticity were blocked by a glucocorticoid receptor antagonist.
- DEX treatment increased CaMKII autophosphorylation and decreased PP1 expression.
- Only DEX treatment disrupted memory retention in passive avoidance tasks.
Conclusions:
- Neonatal DEX treatment adversely affects hippocampal synaptic plasticity and associative memory formation in later life.
- Hydrocortisone (HC) does not appear to cause these neurodevelopmental deficits.
- HC may be a safer alternative to DEX for neonatal CLD treatment.
Abstract:
There is growing concern about long-term neurodevelopmental outcomes after neonatal corticosteroid treatment for chronic lung disease (CLD). Here, we use a protocol with tapering doses of dexamethasone (DEX) or hydrocortisone (HC) proportional to those used in preterm infants to examine the long-term consequences of these treatments on hippocampal synaptic plasticity and associative memory in later life. We found that neonatal DEX, but not HC, treatment impairs long-term potentiation (LTP) but enhances long-term depression (LTD) induction in adolescent rats. The effects of neonatal DEX treatment on LTP and LTD were prevented when the animals were given glucocorticoid receptor antagonist, RU38486, before DEX administration. We also found that neonatal DEX, but not HC, treatment induces a profound increase in the autophosphorylation of a isoform of Ca2+/calmodulin-dependent protein kinase II at threonine-286 and a decrease in the protein phosphatase 1 expression. In addition, only neonatal DEX treatment disrupts memory retention in rats subjected to passive avoidance learning tasks. These results demonstrate that only neonatal DEX treatment alters the hippocampal synaptic plasticity and associative memory formation in later life and thus suggest that HC may be a safer alternative to DEX for the treatment of CLD in the neonatal period.
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