Plastic particles (micro plastics/nano plastics) exist in large quantities in natural environments such as the atmosphere, rivers and soils, enter animals through the respiratory tract or digestive tract, and eventually accumulate in humans, posing potential threats to animal and human health. To date, a large body of literature has reported the toxic effects of plastic particles on adult animals, but their potential toxicity to fetal neuro development is unclear.

Recently, the research team of Ding Yi, associate professor of the School of Animal Science and Technology and the School of Veterinary Medicine of Huazhong Agricultural University, published a research paper on Environment International. This study sheds light on the potential mechanism of action of polystyrene (PS) plastic particles in psychiatric or neurodegenerative diseases.

Autism, schizophrenia, depression, Alzheimer's disease, Parkinson's disease, etc. Belong to human mental diseases or neurodegenerative diseases. Its etiology has not been clearly elucidated, and some studies point it to environmental factors.

In this study, the effects on fetal neuro development were explored by exposing pregnant mice to PS plastic particles with different particle sizes and surface modifications.

Further research found that the micro/nano plastic particles ingested by the pregnant female mice were distributed in the digestive tract, uterus and placenta of the female mice, but only the nanoparticles were accumulated in the fetal thalamus. However, the presence of microplastic particles facilitates the entry of nanoplastic particles into the fetal brain.

Transcriptome sequencing analysis of the thalamus of affected fetuses revealed that plastic particle-induced differentially expressed genes were enriched in oxidative phosphorylation and γ-aminobutyric acid synaptic function-related pathways. In vivo and in vitro experiments confirmed that plastic particles caused oxidative damage and decreased thalamic glutamate decarboxylase 2 (a key enzyme in γ-aminobutyric acid synthesis); damage to thalamic GABAergic neurons resulted in their effects on GABA transmitters in the frontal cortex and amygdala The release was reduced, and the offspring mice showed decreased levels of GABA transmitters and anxiety-like behaviors in adulthood.

Since anxiety-like behaviors are thought to be contributing factors to autism, depression, schizophrenia, Alzheimer's disease, and Parkinson's disease, research provides new insights into the search for potential causes of these disorders.