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Updated: Jul 17, 2026
Restraint to Induce Stress in Mice and Rats
Published on: December 6, 2024
Prenatal restraint stress impairs learning and memory and hippocampal PKCbeta1 expression and translocation in
Jie Wu1, Tian-Bao Song, Yuan-Jie Li
1Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi'an Jiaotong University School of Medicine, Xi'an Shaanxi, 710061, PR China.
Insights
Prenatal stress impairs offspring learning and memory by affecting protein kinase C (PKC) beta1 signaling in the hippocampus. This stress disrupts PKCbeta1 expression and its crucial translocation, leading to cognitive deficits later in life.
Area of Science:
- Neuroscience
- Developmental Psychology
- Molecular Biology
Background:
- Prenatal stress can cause long-term learning and behavioral issues in offspring.
- The precise molecular mechanisms behind these effects remain unclear.
Purpose of the Study:
- To investigate how prenatal stress affects offspring's learning, memory, and hippocampal protein kinase C (PKC) beta1 signaling.
- To examine the impact of prenatal restraint stress on cognitive performance and PKCbeta1 activation in adult rats.
Main Methods:
- Prenatal restraint stress was applied to pregnant rats from gestational days 13-20.
- Offspring cognitive function was assessed using the Morris water maze and passive avoidance training at 1 and 3 months of age.
- Hippocampal expression and translocation of PKCbeta1 were analyzed in stressed and control offspring.
Main Results:
- Prenatally stressed offspring exhibited impaired performance in the Morris water maze and passive avoidance tasks, indicating deficits in learning and memory.
- A significant reduction in both PKCbeta1 protein and mRNA expression was observed in the hippocampus of stressed offspring.
- Unlike controls, stressed offspring did not show the normal training-induced translocation of PKCbeta1 from the cytosol to the membrane in the hippocampus.
Conclusions:
- Prenatal stress disrupts hippocampal PKCbeta1 signaling pathways, including expression and activation.
- Deficient PKCbeta1 signal transduction in the hippocampus is implicated in the learning and memory impairments observed in offspring exposed to prenatal stress.
- These findings highlight a critical molecular mechanism linking early-life stress to long-term cognitive dysfunction.
Abstract:
Prenatal stress results in various learning, behavioral and emotional alterations observed in later life. However, the mechanisms underlying these effects of prenatal stress are not fully understood. In the present study we examined the impact of prenatal stress (an unpredictable restraint stress) during gestational days 13 to 20 on the performance in Morris water maze and passive avoidance training in 1- and 3-month-old rat offspring. The expression and translocation/activation of protein kinase C (PKC) beta1 in the hippocampus of prenatally stressed offspring were also investigated. One-month-old female and male and 3-month-old female prenatally stressed offspring showed longer latency to find the platform and used the inefficient search strategy in the water maze task and showed lower memory score in the passive avoidance training compared with controls. The expression of PKCbeta1 protein and mRNA in the hippocampus of prenatally stressed offspring was dramatically weakened. In the control offspring hippocampus, passive avoidance training induced the PKCbeta1 translocation from the cytosol to the membrane, which, however, was not observed in prenatally stressed offspring. Our results suggest that deficient signal transduction of PKCbeta1 in the hippocampus resulting from prenatal restraint stress may play an important role in the impairment of learning and memory abilities of offspring.
