scholarly journals Maternal Infection Impairs Fetal Brain Development via Choroid Plexus Inflammation

2020 ◽  
Vol 55 (5) ◽  
pp. 519-521
Author(s):  
Britta Engelhardt
Keyword(s):  
Brain Development ◽  
Choroid Plexus ◽  
Fetal Brain ◽  
Maternal Infection ◽  
Fetal Brain Development

scholarly journals Altered Hippocampal Gene Expression and Morphology in Fetal Piglets following Maternal Respiratory Viral Infection

2018 ◽  
Vol 40 (2) ◽  
pp. 104-119 ◽  
Author(s):  
Adrienne M. Antonson ◽  
Bindu Balakrishnan ◽  
Emily C. Radlowski ◽  
Geraldine Petr ◽  
Rodney W. Johnson
Keyword(s):  
Gene Expression ◽  
Viral Infection ◽  
Brain Development ◽  
Hippocampal Neurons ◽  
Protein A ◽  
Fetal Brain ◽  
Respiratory Syndrome Virus ◽  
Maternal Infection ◽  
Ki 67 ◽  
Fetal Brain Development

Maternal infection during pregnancy increases the risk of neurobehavioral problems in offspring. Evidence from rodent models indicates that the maternal immune response to infection can alter fetal brain development, particularly in the hippocampus. However, information on the effects of maternal viral infection on fetal brain development in gyrencephalic species is limited. Thus, the objective of this study was to assess several effects of maternal viral infection in the last one-third of gestation on hippocampal gene expression and development in fetal piglets. Pregnant gilts were inoculated with porcine reproductive and respiratory syndrome virus (PRRSV) at gestational day (GD) 76 and the fetuses were removed by cesarean section at GD 111 (3 days before anticipated parturition). The gilts infected with PRRSV had elevated plasma interleukin-6 levels and developed transient febrile and anorectic responses lasting approximately 21 days. Despite having a similar overall body weight, fetuses from the PRRSV-infected gilts had a decreased brain weight and altered hippocampal gene expression compared to fetuses from control gilts. Notably, maternal infection caused a reduction in estimated neuronal numbers in the fetal dentate gyrus and subiculum. The number of proliferative Ki-67+ cells was not altered, but the relative integrated density of GFAP+ staining was increased, in addition to an increase in GFAP gene expression, indicating astrocyte-specific gliosis. Maternal viral infection caused an increase in fetal hippocampal gene expression of the inflammatory cytokines TNF-α and IFN-γ and the myelination marker myelin basic protein. MHCII protein, a classic monocyte activation marker, was reduced in microglia, while expression of the MHCII gene was decreased in hippocampal tissue of the fetuses from PRRSV-infected gilts. Together, these data suggest that maternal viral infection at the beginning of the last trimester results in a reduction in fetal hippocampal neurons that is evident 5 weeks after infection, when fetal piglets are near full term. The neuronal reduction was not accompanied by pronounced neuroinflammation at GD 111, indicating that any activation of classic neuroinflammatory pathways by maternal viral infection, if present, is mostly resolved by parturition.

New normal range of fetal cavum septum pellucidum in the second trimester of gestation

2020 ◽  
Author(s):  
M.V. Medvedev, O.I. Kozlova, À.Yu. Romanova
Keyword(s):  
Brain Development ◽  
Reference Range ◽  
Fetal Brain ◽  
Septum Pellucidum ◽  
Second Trimester ◽  
Normal Range ◽  
Cavum Septum Pellucidum ◽  
New Normal ◽  
Biparietal Diameter ◽  
Fetal Brain Development

Fetal brain was retrospectively evaluated in 418 normal fetuses at 16–28 weeks of gestation. The multiplanar mode to obtain the axial cerebral plane and measured the width of the cavum septum pellucidum (CSP) and biparietal diameter (BD). All measurements of CSP were done from as the widest diameter across both borders in an inter-to inter fashion. The CSP width is increasing at second trimester of gestation. Normal range plotted on the reference range (mean, 5th and 95th percentiles) of fetal width CSP by measuring of its size may be useful for assessment of fetal brain development in the second trimester of gestation.

scholarly journals CB1 antagonism increases excitatory synaptogenesis in a cortical spheroid model of fetal brain development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alexis Papariello ◽  
David Taylor ◽  
Ken Soderstrom ◽  
Karen Litwa
Keyword(s):  
Brain Development ◽  
Spontaneous Activity ◽  
Microelectrode Array ◽  
Cannabinoid Receptor ◽  
Fetal Brain ◽  
Endocannabinoid System ◽  
Autism Spectrum ◽  
Nervous System Development ◽  
Inhibitory Synapses ◽  
Fetal Brain Development

AbstractThe endocannabinoid system (ECS) plays a complex role in the development of neural circuitry during fetal brain development. The cannabinoid receptor type 1 (CB1) controls synaptic strength at both excitatory and inhibitory synapses and thus contributes to the balance of excitatory and inhibitory signaling. Imbalances in the ratio of excitatory to inhibitory synapses have been implicated in various neuropsychiatric disorders associated with dysregulated central nervous system development including autism spectrum disorder, epilepsy, and schizophrenia. The role of CB1 in human brain development has been difficult to study but advances in induced pluripotent stem cell technology have allowed us to model the fetal brain environment. Cortical spheroids resemble the cortex of the dorsal telencephalon during mid-fetal gestation and possess functional synapses, spontaneous activity, an astrocyte population, and pseudo-laminar organization. We first characterized the ECS using STORM microscopy and observed synaptic localization of components similar to that which is observed in the fetal brain. Next, using the CB1-selective antagonist SR141716A, we observed an increase in excitatory, and to a lesser extent, inhibitory synaptogenesis as measured by confocal image analysis. Further, CB1 antagonism increased the variability of spontaneous activity within developing neural networks, as measured by microelectrode array. Overall, we have established that cortical spheroids express ECS components and are thus a useful model for exploring endocannabinoid mediation of childhood neuropsychiatric disease.

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

Fetal brain development of twins assessed in utero by ultrasound: implications for schizophrenia

1996 ◽  
Vol 19 (2-3) ◽  
pp. 141-149 ◽  
Author(s):  
John H. Gilmore ◽  
Diana O. Perkins ◽  
Mark A. Kliewer ◽  
Marvin L. Hage ◽  
Susan G. Silva ◽  
...  
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
In Utero ◽  
Fetal Brain Development
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