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Updated: Jun 29, 2026

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
Published on: March 2, 2018
Perspective: Chicken Models for Studying the Ontogenetic Origin of Neuropsychiatric Disorders
Xiaohong Huang1,2, Heng-Wei Cheng2,3
1Institute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao 266071, China.
Insights
Prenatal exposure to substances affects fetal brain development and behavior. Chicken embryos offer a viable model to study these effects and the origins of neuropsychiatric disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Microbiology
Background:
- Nutrients and xenobiotics cross the blood-placenta barrier, impacting fetal neurodevelopment and the microbiota-gut-brain axis.
- Investigating prenatal exposure effects is challenging in humans and rodents due to ethical and biological constraints.
- The maternal-fetal transfer of microbes shapes the initial gut microbiome, complicating rodent model studies.
Purpose of the Study:
- To explore the mechanisms by which maternal risk factors reprogram the microbiota-gut-brain axis.
- To investigate the long-term effects of prenatal exposure on psychosocial behaviors.
- To establish chicken embryos as a suitable alternative model for studying fetal exposure effects on neurogenesis and neuropsychiatric disorders.
Main Methods:
- Utilizing chicken embryos for deposition assessment and mechanistic studies due to accessibility and controlled development.
- Leveraging the social predisposition of chickens to study behavioral responses shortly after hatching.
- Comparing chicken embryos to human and rodent models for assessing fetal exposure impacts.
Main Results:
- Chicken embryos provide a unique model for assessing nutrient and xenobiotic deposition in the developing brain.
- The model allows for in vivo experimental manipulation to study neurogenesis and the origins of neuropsychiatric disorders.
- Chicken embryos circumvent the confounding factor of maternal-fetal microbial transfer present in rodent models.
Conclusions:
- Chicken embryos are a valuable alternative model for studying the effects of prenatal exposure on neurodevelopment.
- This model facilitates research into the ontogenetic origins of behaviors and neuropsychiatric disorders.
- The findings support the use of chicken embryos for mechanistic studies on fetal exposure and brain development.
Abstract:
Nutrients and xenobiotics cross the blood-placenta barrier, potentially depositing in the fetal brain. The prenatal exposure affects the neuroendocrine and microbial development. The mechanism underlying maternal risk factors reprograming the microbiota-gut-brain axis with long-term effects on psychosocial behaviors in offspring is not clear. In humans, it is not possible to assess the nutrient or xenobiotic deposition in the fetal brain and gastrointestinal system for ethical reasons. Moreover, the maternal-fetal microbe transfer during gestation, natural labor, and breast-feeding constitutes the initial gut microbiome in the progeny, which is inevitable in the most widely utilized rodent models. The social predisposition in precocial birds, including chickens, provides the possibility to test behavioral responses shortly after being hatched. Hence, chickens are advantageous in investigating the ontogenetic origin of behaviors. Chicken embryos are suitable for deposition assessment and mechanistic study due to the accessibility, self-contained development, uniform genetic background, robust microbiota, and easy in vivo experimental manipulation compared to humans and rodents. Therefore, chicken embryos can be used as an alternative to the rodent models in assessing the fetal exposure effect on neurogenesis and investigating the mechanism underlying the ontogenetic origin of neuropsychiatric disorders.

