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Published on: December 29, 2014
Environmental Enrichment Protects Offspring of a Rat Model of Preeclampsia from Cognitive Decline
Huiqing Lu1,2, Lili Gong1,2, Huangfang Xu1,2
1Obstetrics and Gynecology Hospital, Fudan University, No.419 Fangxie Rd. Huangpu Division, Shanghai, 200011, China.
Insights
Environmental enrichment improved cognitive deficits in offspring from a preeclampsia rat model. This intervention enhanced hippocampal neurogenesis and synaptic plasticity while reducing apoptosis and inflammation.
Area of Science:
- Neuroscience
- Developmental Biology
- Reproductive Medicine
Background:
- Preeclampsia impacts 5-7% of pregnancies, causing adverse outcomes for mothers and offspring.
- Offspring of preeclamptic mothers exhibit long-term cognitive deficits, necessitating effective interventions.
- Current strategies to mitigate these cognitive deficits remain under investigation.
Purpose of the Study:
- To investigate if early-life environmental enrichment (EE) can restore cognitive function in offspring of preeclampsia rat models.
- To elucidate the cellular and molecular mechanisms underlying EE's cognitive benefits.
Main Methods:
- A rat model of preeclampsia was induced using L-NAME.
- Cognitive abilities were assessed using the Morris water maze and Novel Object Recognition (NOR) task.
- Hippocampal neurogenesis, apoptosis, synaptic plasticity, VEGF, and inflammatory cytokines were analyzed via immunofluorescence, qRT-PCR, and ELISA.
Main Results:
- L-NAME induced preeclampsia symptoms and impaired offspring cognitive and memory functions.
- Offspring exhibited reduced hippocampal neurogenesis, impaired synaptic plasticity, increased apoptosis, and heightened hippocampal inflammation.
- EE intervention successfully improved cognitive abilities, enhanced neurogenesis and synaptic plasticity, and reduced apoptosis and inflammation.
Conclusions:
- Environmental enrichment effectively reverses cognitive impairment in offspring of preeclampsia models.
- EE normalizes hippocampal neurogenesis, synaptic plasticity, apoptosis, and inflammatory balance.
- This study highlights EE as a potential therapeutic strategy for cognitive deficits in offspring exposed to preeclampsia in utero.
Abstract:
Preeclampsia affects 5-7% of all pregnancies and contributes to adverse pregnancy and birth outcomes. In addition to the short-term effects of preeclampsia, preeclampsia can exert long-term adverse effects on offspring. Numerous studies have demonstrated that offspring of preeclamptic women exhibit cognitive deficits from childhood to old age. However, effective ways to improve the cognitive abilities of these offspring remain to be investigated. The aim of this study was to explore whether environmental enrichment in early life could restore the cognitive ability of the offspring of a rat model of preeclampsia and to investigate the cellular and molecular mechanisms by which EE improves cognitive ability. L-NAME was used to establish a rat model of preeclampsia. The spatial learning and memory abilities and recognition memory of 56-day-old offspring were evaluated by the Morris water maze and Novel object recognition (NOR) task. Immunofluorescence was performed to evaluate cell proliferation and apoptosis in the DG region of the hippocampus. qRT-PCR was performed to examine the expression levels of neurogenesis-associated genes, pre- and postsynaptic proteins and inflammatory cytokines. An enzyme-linked immune absorbent assay was performed to evaluate the concentration of vascular endothelial growth factor (VEGF) and inflammatory cytokines in the hippocampus. The administration of L-NAME led to increased systolic blood pressure and urine protein levels in pregnant rats. Offspring in the L-NAME group exhibited impaired spatial learning ability and memory as well as NOR memory. Hippocampal neurogenesis and synaptic plasticity were impaired in offspring from the L-NAME group. Furthermore, cell apoptosis in the hippocampus was increased in the L-NAME group. The hippocampus was skewed to a proinflammatory profile, as shown by increased inflammatory cytokine levels. EE improved the cognitive ability of offspring in the L-NAME group and resulted in increased hippocampal neurogenesis and synaptic protein expression levels and decreased apoptosis and inflammatory cytokine levels. Environmental enrichment resolves cognitive impairment in the offspring of a rat model of preeclampsia by improving hippocampal neurogenesis and synaptic plasticity and normalizing the apoptosis level and the inflammatory balance.
