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Published on: December 14, 2014
Exposure to prenatal stress enhances the development of seizures in young rats
Lihle Qulu1, Willie M U Daniels, Musa V Mabandla
1Department of Human Physiology, College of Health Sciences, University of KwaZulu-Natal, Durban 4000, South Africa.
Insights
Prenatal stress in rats exacerbated febrile seizures in offspring, increasing seizure severity and interleukin-1 beta (IL-1β) levels. This suggests prenatal stress impacts neurological development and inflammation, contributing to febrile seizure outcomes.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Febrile seizures are common in young children, linked to rapid temperature increases.
- Interleukin-1 beta (IL-1β), a pro-inflammatory cytokine, is implicated in febrile seizure development.
- Prenatal stress exposure can worsen neurological disorders in offspring.
Purpose of the Study:
- To investigate the effect of prenatal stress on febrile seizure exacerbation in rat offspring.
- To determine the role of interleukin-1 beta (IL-1β) in stress-induced febrile seizures.
Main Methods:
- Pregnant Sprague-Dawley rats were exposed to restraint stress from gestational day 14.
- Offspring received lipopolysaccharide (LPS) and kainic acid (KA) injections on postnatal day 14.
- Plasma IL-1β levels were measured on postnatal day 21.
Main Results:
- LPS and KA induced seizure activity and elevated plasma IL-1β levels.
- Prenatal stress led to more severe seizures and higher IL-1β levels in offspring.
- Prenatal stress alone increased IL-1β levels; combined stress and LPS/KA yielded the highest IL-1β.
Conclusions:
- Prenatal stress exacerbates febrile seizures in rat offspring.
- Elevated IL-1β levels are associated with stress-induced febrile seizure severity.
- IL-1β may be a key mediator in the development of febrile seizures following prenatal stress.
Abstract:
A febrile seizure is a neurological disorder that occurs following an infection that results in a rapid rise in body temperature. It commonly affects 3-5% of children between the ages of 3 months and 5 years. Interleukin-1 beta IL-1β a pro-inflammatory cytokine has been suggested to play a role in the manifestation of febrile seizures. There is evidence suggesting that neurological disorders can be exacerbated in an offspring that was exposed to stress prenatally. The aim of our study was therefore to investigate whether febrile seizures are exacerbated in the offspring of rats that were prenatally stressed. The offspring of pregnant Sprague-Dawley dams were used in the study. Prenatal stress consisted of exposing the pregnant dams to 45 min of restraint, 3 times per day with 3 h intervals in-between, for 7 days starting on gestational day 14 (GND14). On postnatal day (PND) 14, the pups were injected with lipopolysaccharide (LPS, 200 μg/kg, i.p.) followed 2.5 h later by an i.p. injection of kainic acid (KA, 1.75 mg/kg). All the animals were decapitated on PND 21. Trunk blood was collected to detect plasma interleukin-1beta (IL-1β) levels in the various groups. Our data showed that i.p. injections of LPS followed by KA led to the development of seizure activity that was associated with increased plasma IL-1β levels. Prior exposure to prenatal stress resulted in the development of advanced stages of seizure development, leading to an exaggerated seizure response. Prenatal stress alone also led to elevated plasma IL-1β levels, while previously stressed animals receiving LPS and KA yielded the highest plasma levels of IL-1β levels. Our data therefore shows that IL-1β levels may play an important role in the development of febrile seizures.
