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Updated: May 29, 2026
Restraint to Induce Stress in Mice and Rats
Published on: December 6, 2024
Prenatal exposure to restraint or predator stresses attenuates field excitatory postsynaptic potentials in infant
Ehsan Saboory1, Ramin Ahmadzadeh, Shiva Roshan-Milani
1Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Insights
Prenatal stress in rats, including restraint and predator exposure, impairs hippocampal synaptic potentiation. This stress also increases seizure susceptibility and mortality in infant rats.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Stress Research
Background:
- Stress exposure is known to alter synaptic plasticity and can precipitate seizures.
- Prenatal stress effects on offspring's neurological development and seizure susceptibility are not fully understood.
Purpose of the Study:
- To investigate the impact of prenatal restraint and predator stress on hippocampal synaptic potentiation in infant rats.
- To determine if prenatal stress influences seizure susceptibility in early life.
Main Methods:
- Pregnant Wistar rats were exposed to restraint or predator stress on specific gestation days.
- Blood corticosterone levels were measured in dams and pups.
- Hippocampal slices were analyzed for field excitatory postsynaptic potentials (fEPSP) on postnatal day 15.
- Seizure susceptibility was assessed using pilocarpine administration on postnatal day 25, with mortality rates recorded.
Main Results:
- Both restraint and predator stress significantly elevated corticosterone (COS) levels in dams and pups.
- Prenatal stress exposure led to a significant decrease in fEPSP amplitude and slope in the hippocampal CA1 area.
- Stressed groups exhibited a significantly higher mortality rate following pilocarpine administration compared to controls.
Conclusions:
- Exposure to prenatal stress, evidenced by elevated corticosterone levels, reduces hippocampal synaptic potentiation in infant rats.
- Prenatal stress increases the mortality rate associated with seizures in infant rats, suggesting potential long-term effects on seizure susceptibility and prognosis.
Abstract:
Exposure to stress is known to change synaptic plasticity and results in long-term depression; further, this stress precipitates seizures. In the study described here, the prenatal restraint and predator stress models were used to test the hypothesis that indirect prenatal stresses influence hippocampal synaptic potentiation and may affect seizures susceptibility in infant rats. Pregnant female Wistar rats were divided into 3 groups: control, restraint-stressed, and predator-stressed groups. Both stressed groups were exposed to the stressor on gestation days 15, 16, and 17. The restraint stress involved 1-h sessions twice daily in a Plexiglas tube and the predator stress involved 2-h sessions once daily in a cage placed within the visual range of a caged cat. Blood corticosterone (COS) levels were measured in different time points. Hippocampal slices were prepared and field excitatory postsynaptic potentials (fEPSP) were studied on postnatal day 15. Pilocarpine was administered on postnatal day 25 and mortality rates were measured after 2 and 24h. Restraint and predator stresses resulted in significantly elevated COS blood levels in dams and pups. Both the amplitude and slope of fEPSP in the CA1 area decreased significantly in the stressed groups as compared to the control. Prenatal restraint and predator stresses significantly increased the fatal effect of pilocarpine at 24h after injection. Exposure to prenatal stresses and COS blood levels elevation reduce hippocampal synaptic potentiation and increase mortality rate of seizure in infant rats and may affect on later seizure susceptibility and prognosis.
