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Disrupted senses and social cues: Impacts of nanoplastics and methylmercury on zebrafish neurodevelopment
Summary
Researchers exposed developing zebrafish to nanoplastics alone and in combination with methylmercury to study effects on brain development and behavior. Nanoplastics accumulated in sensory organs called neuromasts during early development and disrupted the startle response and social behavior in juvenile fish. The study suggests that nanoplastics can impair neurodevelopment and may worsen the toxic effects of co-occurring environmental contaminants like mercury.
With the advancement of analytical techniques and the global increase in plastic pollution, nanoplastics (NPs) have been increasingly detected across all ecosystems and in deep tissues, including the human brain. Notably, NPs are capable of acting as vectors for co-contaminants such as heavy metals, raising concerns about their combined toxicity. In this study, zebrafish (Danio rerio) were exposed to 250 nm polystyrene NPs (1000 µg/L), either alone or in combination with 10 µg/L of methylmercury (MeHg), during the first 30 days of development. Neuromast development and vibrational startle response were evaluated at both larval and juvenile stages, while brain histopathology and social behaviour were assessed at the juvenile stage. NPs were found to accumulate in neuromasts during early larval stages, temporarily impairing their development and affecting the startle response to vibrational stimuli. NPs alone also altered social behaviour, enhancing body contact frequency and duration, yet resulting in looser shoal cohesion. Co-exposure with MeHg led to more severe behavioural impairments, including diminished social interactions, reduced responses to stress, and delayed neuromast development. Despite these functional changes, histopathological examination revealed minimal structural alterations in the central nervous system, except for significant accumulation of glial cells in the optic tectum following NPs-exposure. These findings suggest that behavioural disruptions are likely mediated by impaired peripheral sensory inputs and altered neurotransmission rather than apparent neuroanatomical damages.