Related Experiment Video

Updated: Aug 15, 2025

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
03:19

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes

Published on: June 28, 2024

483

Maternal Hyperhomocysteinemia Disturbs the Mechanisms of Embryonic Brain Development and Its Maturation in Early

Dmitrii S Vasilev1, Anastasiia D Shcherbitskaia1,2, Natalia L Tumanova1

  • 1I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, 194223 St. Petersburg, Russia.

Cells
|January 8, 2023
PubMed

Insights

Prenatal hyperhomocysteinemia (PHHC) in rats delays male pup maturation and brain development. This condition disrupts neurogenesis, neuronal migration, and neural tissue maturation, impacting motor function.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Toxicology

Background:

  • Maternal hyperhomocysteinemia disrupts placental blood flow, potentially harming fetal brain development.
  • Prenatal hyperhomocysteinemia (PHHC) is linked to adverse neurodevelopmental outcomes.

Purpose of the Study:

  • To investigate the effects of PHHC on neuronal migration, neural tissue maturation, and signaling molecule expression in the rat fetal brain.
  • To understand the molecular mechanisms underlying PHHC-induced developmental delays.

Main Methods:

  • Induced maternal hyperhomocysteinemia in rats via methionine administration during pregnancy.
  • Assessed neurodevelopmental delays using behavioral tests and ultrastructural analysis of cortical and hippocampus tissues.
  • Analyzed gene and protein expression of key developmental and apoptotic markers (e.g., Bdnf, Kdr, SEMA3E, caspases).

Main Results:

  • PHHC induced developmental delays in male rat pups, evident in behavioral tests and tissue ultrastructure.
  • PHHC impaired neuroblast generation and radial migration into the cortical plate.
  • Altered expression of Bdnf, Kdr, and SEMA3E, alongside increased caspase-3 activity, suggests disrupted neuronal viability, maturation, and apoptosis.

Conclusions:

  • PHHC significantly disturbs early brain development mechanisms in rats.
  • The observed delays in brain tissue maturation and motor function formation are consequences of PHHC.
  • Findings highlight the critical role of homocysteine levels during pregnancy for normal fetal brain development.

Keywords:
caspaseelectron microscopyhippocampushomocysteinematrix metalloproteinaseneocortexneurodegenerationneurotrophinsratsemaphorin

More Related Videos

Author Spotlight: Collecting the Brain and Serum from the Same Mice Fetus to Study Brain Tumor Development05:44

Author Spotlight: Collecting the Brain and Serum from the Same Mice Fetus to Study Brain Tumor Development

Published on: May 17, 2024

681
Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic PolyI:C07:13

Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic PolyI:C

Published on: March 25, 2016

18.6K

Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
2.6K
Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...
57.4K
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
221