Maternal Infections Impact Newborn Brain Development: Research
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Synopsis
A study from European researchers reveals that maternal infections during pregnancy can have long-term consequences on the brain development of newborns, potentially leading to neurodevelopmental disorders.
Key Takeaways
- Maternal infections can disrupt brain function in offspring.
- Research highlights the role of hippocampal neurons in memory and cognition.
- Inflammation during pregnancy affects neuronal excitability.
- Study suggests a link between prenatal inflammation and disorders like autism.
- Male offspring may be more affected than females.
New Delhi, March 18 (NationPress) A groundbreaking study by a team of European researchers has revealed significant evidence that maternal infections during pregnancy can lead to enduring effects on the brain function of offspring. This research, published in the peer-reviewed journal Brain Medicine, could have serious implications for neurodevelopmental and psychiatric conditions such as autism, schizophrenia, and depression.
The research team from the Slovak Academy of Sciences in Slovakia examined the effects of maternal immune activation (MIA) on the hippocampal pyramidal neurons of newborn rat offspring.
The hippocampus is a vital brain area that plays a role in memory, emotion, and cognition. The study found that inflammation during pregnancy significantly hampers neuronal excitability, raising the risk of developing neurodevelopmental disorders linked to maternal infections.
Dr. Eliyahu Dremencov from the institute stated, "Maternal infections are a known risk factor for conditions like autism, schizophrenia, and depression."
He further explained, "Our research indicates that early changes in hippocampal neuron function may be a crucial factor connecting prenatal inflammation to these disorders."
During pregnancy, infections activate the immune system, releasing cytokines—chemical messengers that can cross the placenta and affect fetal brain development.
In their study, the researchers used a well-established animal model, inducing MIA in pregnant rats using lipopolysaccharide (LPS), a bacterial component that activates the immune response. They subsequently assessed the hippocampal neurons of the newborns to evaluate the effects of prenatal immune activation on their excitability.
Lead author Dr. Lucia Moravcikova noted, "We found that neurons from MIA-exposed offspring had a markedly higher activation threshold, slower response times, and decreased firing rates."
"This indicates a disruption in glutamatergic neurotransmission, which is essential for learning, memory, and emotional regulation," Moravcikova added.
The team also observed significant alterations in hippocampal neuron function in newborns exposed to MIA.
They noted that these neurons required stronger stimuli to activate, indicating reduced excitability; they also responded more slowly to stimulation, which could affect signal transmission.
Importantly, male offspring exhibited a greater decrease in spontaneous neuronal activity, potentially explaining the higher prevalence of conditions such as autism and schizophrenia in males.
