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Published on: February 9, 2024
Prenatal stress promotes development of spasms in infant rats
Mi-Sun Yum1, Tamar Chachua, Jana Velíšková
1Department of Pediatrics, Asan Medical Center, Seoul, Republic of Korea.
Insights
Prenatal stress in rats increased susceptibility to infantile spasms triggered by N-methyl-d-aspartate (NMDA). Long-term adrenocorticotropic hormone (ACTH) treatment protected against these spasms.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Infantile spasms are a severe epilepsy syndrome.
- Prenatal stress is linked to increased risk of infantile spasms.
- Animal models are crucial for understanding spasm development.
Purpose of the Study:
- To investigate the impact of prenatal stress on infantile spasm susceptibility.
- To explore the role of adrenocorticotropic hormone (ACTH) in modulating spasms.
Main Methods:
- Developed a rat model of infantile spasms using prenatal restraint stress.
- Administered N-methyl-d-aspartate (NMDA) to trigger spasms.
- Evaluated the effects of acute and long-term ACTH administration.
Main Results:
- Prenatal stress accelerated spasm onset and increased NMDA-triggered spasm frequency.
- Acute ACTH had no effect on spasms.
- Long-term ACTH pretreatment increased latency to onset and reduced spasm number.
Conclusions:
- Prenatal stress enhances susceptibility to NMDA-induced spasms.
- Long-term ACTH administration demonstrates a protective effect, mirroring human conditions.
- Minimizing prenatal stress is crucial for infant health.
Abstract:
We have developed a new model of cryptogenic infantile spasms with prenatal betamethasone brain priming to increase susceptibility to development-specific spasms triggered by N-methyl-d-aspartate (NMDA). A recent clinical study linked severe prenatal stress to increased risk for development of infantile spasms. Here, we determined whether prenatal restraint stress (2 × 45 min) in rats on gestational day 15 would increase susceptibility to develop spasms on postnatal day 15. Prenatal stress significantly accelerated onset and increased number of NMDA-triggered spasms compared to handled controls. A single adrenocorticotropic hormone (ACTH or corticotropin) dose delivered acutely had no effects, whereas long-term (3 day) ACTH pretreatment significantly increased latency to onset and decreased number of spasms (an effect similar to that in the human condition). Our data support the notion that extra care should be provided during pregnancy to minimize stress.
