Topic: Prenatal alcohol exposure

Prenatal alcohol exposure (PAE) leads to immune system dysfunction and increased susceptibility to autoimmune diseases. To explore potential mechanisms by which PAE induces neuroimmune dysfunction, the current study examined the impact of PAE on toll-like receptor 4 (TLR4) and TLR7/8 activation. Pregnant rats were divided into two groups: PAE - liquid ethanol diet ad libitum, and CON - pelleted control diet ad libitum. Male and female offspring were challenged in adulthood with LPS (40 µg/kg; activates TLR4), R848 (1 mg/kg; activates TLR7/8), or DMSO (vehicle), followed by brain sample collect

Prenatal alcohol exposure (PAE) impairs the “placenta–brain” axis that controls foetal brain angiogenesis. Placental growth factor (PlGF) has been identified as a proangiogenic messenger between these two organs. CD146, a partner of the VEGFR-1/2 signalosome, is involved in placental angiogenesis and exists as a soluble circulating form. The aim of the study was to investigate whether placental CD146 may contribute to brain vascular defects described in foetal alcohol spectrum disorder. In human placenta, the CD146 is expressed in developing villi and membrane and soluble CD146 forms are diffe

Although alcohol consumption during pregnancy is a major cause of behavioral and learning disabilities, most FASD infants remain late- or even misdiagnosed. Neuroplacentology has emerged as a new field of research focusing on the role of the placenta in fetal brain development. Several studies focusing on the pro-angiogenic factor PlGF have reported that prenatal alcohol exposure (PAE) dysregulates a functional placenta–cortex axis, leading to neurovascular-related defects. Here, we provide the first transcriptomic “placenta–cortex” signature of the effects of PAE on fetal angiogenesis. Whole

Background: Prenatal alcohol exposure (PAE) induces a wide range of neurodevelopmental disabilities grouped under the term fetal alcohol spectrum disorders (FASD). The effects of PAE on brain development are dependent on complex long-lasting neurochemical events, including modification of glutamate receptors. Here, we explored whether PAE may affect the functional connectivity and, further, the molecular composition of the glutamatergic synapses in the prefrontal cortex (PFC) of adolescent mice and its effect on social behaviors.Methods: We generated an in vivo model of PAE, by exposing C57Bl/

Ethanol (EtOH) exposure during pregnancy can induce a range of physical, learning, and behavioral disorders in the newborn clinically referred as Fetal Alcohol Spectrum Disorder (FASD). Unfortunately, FASD is poorly understood, and the underlying mechanisms are not fully known. Here, we studied the role of AMPA receptors (AMPARs) in in vitro and in vivo models of prenatal alcohol exposure (PAE). For the in vitro study, immature rat organotypic hippocampal slices were exposed to EtOH (150 mM) for 7 days followed by 24 hours of withdrawal. For the in vivo study, female C57/Bl6 mice were exposed