Effects of microplastics exposure on learning and memory in mice and its mechanism
10.16098/j.issn.0529-1356.2024.05.004
- VernacularTitle:微塑料暴露对小鼠学习记忆的影响及其作用机制
- Author:
Xin-Ze JIANG
1
;
Qiang LIU
;
Xu SUN
;
Jiang-Shan HOU
;
Rui MA
;
Mei CHENG
;
Yu-Long WU
Author Information
1. 滨州医学院基础医学院病原生物学系,山东烟台 264003
- Keywords:
Microplastics;
Learning;
Memory;
Brain-derived neurotrophic factor;
Tyrosine receptor kinase B;
N-methyl-D-aspartate receptor subtype 2B;
Neurogenesis;
Western blotting;
Mouse
- From:
Acta Anatomica Sinica
2024;55(5):541-546
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of microplastic(MPs)exposure on learning and memory in mice,and its mechanism by observing the protein expression of brain-derived neurotrophic factor(BDNF)/tyrosine receptor kinase B(TrkB)/N-methyl-D-aspartate receptor subtype 2B(NR2B)signaling pathway and neurogenesis.Methods Forty male C57BL/6 mice were randomly divided into control group(Ctrl)and microplastics exposure group(MPs).Mice in MPs group were treated with 0.3 mg/(kg·d)microplastics,administered by gavage at a volume of 200 μl for 30 consecutive days.Morris water maze test was used to evaluate the spatial learning and memory ability of mice.Western blotting was used to detect the protein levels of BDNF,TrkB and NR2B in hippocampus of mice.Immunofluorescent staining was used to observe the number of doublecortin(DCX)and neuronal nuclei antigen(NeuN)positive cells in the hippocampus of mice to evaluate hippocampal neurogenesis.Results Compared with the control group,the ability of learning and memory decreased significantly in MPs group mice(P＜0.01).The expression levels of BDNF,TrkB and NR2B in the hippocampus of MPs group mice were significantly lower than those of control group(P＜0.05).The number of DCX and NeuN positive cells in the hippocampus of MPs group was significantly lower than that of control group(P＜0.01).Conclusion MPs exposure induces learning and memory impairment which may be related to inhibiting BDNF/TrkB/NR2B signaling pathway and reducing hippocampal neurogenesis.
