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Neurotoxic effects of nanoplastics exposure on depression-like behavior and cognitive function in mice under chronic unpredictable mild stress.
Summary
Scientists fed mice tiny plastic particles (nanoplastics) and found they worsened depression-like behavior and memory problems, especially in mice already under chronic stress—mimicking the toll of everyday stress in humans. The nanoplastics appeared to damage brain cells in the hippocampus (the brain's memory center) by disrupting a key protein that helps neurons grow and communicate. While this study was in mice, it raises concerns about how the growing amount of plastic particles in our food, water, and air might affect mental health and brain function in people, particularly those already dealing with chronic stress.
The aim was to investigate the effects of gavage exposure to nanoplastics (NPs) on cognitive decline and depression-like behavior was in-vestigated in mice subjected to chronic unpredictable mild stress (CUMS). BALB/c mice were randomly assigned to four experimental groups: Control (Ctrl), nanoplastics (NPs), Mod (subjected to CUMS), and NPs+Mod (nano-plastics + CUMS). We evaluated the role of the brain-derived neurotrophic fac-tor (BDNF) and its receptor, the tyrosine kinase receptor B (TrkB), signaling pathway in the hippocampus of mice. Behavioral assessments included the su-crose preference test, the open field test, the forced swim test, and the Morris water maze. Nissl staining was used to assess hippocampal neuronal morphol-ogy. BDNF and TrkB mRNA levels and protein expression in the hippocampus were measured by qPCR and Western blotting, respectively. Mice in the NPs, Mod, and NPs+Mod groups showed reduced body weight, lower sucrose pref-erence, poorer performance in the open field test, and prolonged immobility in the forced swim test. Additionally, there was a reduction in hippocampal neurons and deficits in spatial learning and memory compared with the con-trol group. BDNF mRNA and TrkB protein levels were decreased. Compared with the Mod group, the NPs+Mod group exhibited increased depression-like behaviors and cognitive impairments, greater hippocampal neuronal damage, and further reductions in BDNF and TrkB mRNA and protein levels. In conclu-sion, NP exposure has neurotoxic properties that can exacerbate CUMS-induced depression-like behavior and cognitive deficits, likely by further suppressing the hippocampal BDNF/TrkB signaling pathway.