Cited by 127Memory and Neural MechanismsStress Responses and CortisolNeuroscience and Neuropharmacology Research

Enriched environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress

Yang, Jianli, Hou, Cailan, Ma, Ning, Liu, Jun, Zhang, Yan, Zhou, Jiansong, Xu, Lin, Li, Lingjiang·2007·Neurobiology of Learning and Memory

Abstract

Prenatal stress can cause long-term effects on cognitive functions in offspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether enriched environment treatment (EE) in early postnatal periods can cause a recovery from these deficits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1s, 2-3 min apart) in 30 min per day at gestational day 13-19. After weaning at postnatal day 22, experimental offspring were given the enriched environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the effects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deficits induced by prenatal stress were recovered by enriched environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deficit, prenatal stress and enriched environment treatment. Enriched environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.

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Crossref · 10.1016/j.nlm.2006.09.001

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Authors
Yang, J., Hou, C., Ma, N., Liu, J., Zhang, Y., Zhou, J., Xu, L., & Li, L.
Affiliations
Central South University (CN)
Corresponding author
  • Xu, Lin
  • Li, Lingjiang
Venue
Neurobiology of Learning and Memory
Publisher
Elsevier BV
Published
2007-02
Volume
87
Issue
2
Pages
257-263
ISSN
1074-7427 (ISSN-L)
OpenAlex
W1980458726
Cited by
127
References
38
Citations by year
2026: 2 · 2025: 2 · 2023: 4 · 2022: 4 · 2021: 2 · 2020: 9 · 2019: 8 · 2018: 6 · 2017: 7 · 2016: 12 · 2015: 6 · 2014: 7 · 2013: 5 · 2012: 11
FWCI
3.88
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Learning and Memory (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
prenatal stress, environmental enrichment, hippocampal synaptic plasticity, long-term potentiation, long-term depression, CA1 region, spatial learning and memory, cognitive impairment, acute stress, footshock stress, rat offspring
MeSH terms
Animals, Behavior, Animal, Cognition Disorders, Environment, Female, Hippocampus, Neuronal Plasticity, Pregnancy, Prenatal Exposure Delayed Effects, Reaction Time, Stress, Psychological, Rats, Wistar, Maze Learning, Excitatory Postsynaptic Potentials, Rats, In Vitro Techniques

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