Publications by authors named "Muna L Hilal"

Article Synopsis
  • Autism Spectrum Disorder (ASD) is influenced by genetic, epigenetic, and environmental factors, particularly mutations in the FMR1 gene linked to Fragile X Syndrome (FXS).
  • The study used a mouse model to examine how a simulated viral infection (maternal immune activation, MIA) during pregnancy affects the development of ASD-like behaviors in offspring, finding that such exposure led to these behaviors only when it occurred in the womb.
  • MIA activation influenced the mGluR1/5-mTOR signaling pathway, impacting learning and memory processes in the hippocampus, but combining MIA with the Fmr1 mutation did not worsen autistic traits, indicating a complex interaction between genetic and environmental factors.
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Status epilepticus (SE) is a condition in which seizures are not self-terminating and thereby pose a serious threat to the patient's life. The molecular mechanisms underlying SE are likely heterogeneous and not well understood. Here, we reveal a role for the RNA-binding protein Fragile X-Related Protein 2 (FXR2P) in SE.

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Planar cell polarity (PCP) signaling is well known to play a critical role during prenatal brain development; whether it plays specific roles at postnatal stages remains rather unknown. Here, we investigated the role of a key PCP-associated gene scrib in CA1 hippocampal structure and function at postnatal stages. We found that Scrib is required for learning and memory consolidation in the Morris water maze as well as synaptic maturation and NMDAR-dependent bidirectional plasticity.

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Extensive evidence suggests that long term dietary n-3 polyunsaturated fatty acids (PUFAs) deficiency results in altered emotional behaviour. We have recently demonstrated that n-3 PUFAs deficiency induces emotional alterations through abnormal corticosterone secretion which leads to altered dendritic arborisation in the prefrontal cortex (PFC). Here we show that hypothalamic-pituitary-adrenal (HPA) axis feedback inhibition was not compromised in n-3 deficient mice.

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