Progressive impairment of learning and memory in adult zebrafish treated by Al2O3 nanoparticles when in embryos

Abstract

Al₂O₃ Nanoparticles (Al₂O₃-NPs) have been widely used because of their unique physical and chemical properties, and Al₂O₃-NPs can be released into the environment directly or indirectly. Our previous research found that 13 nm Al₂O₃-NPs can induce neural cell death and autophagy in primarily cultured neural cells in vitro. The aim of this study was to determine where Al₂O₃-NPs at 13 nm particle size can cause neural cells in vivo and assess related behavioural changes and involved potential mechanisms. Zebrafish from embryo to adult were selected as animal models. Learning and memory as functional indicators of neural cells in zebrafish were measured during the development from embryo to adult. Our results indicate that Al₂O₃-NPs treatment in zebrafish embryos stages can cause the accumulation of aluminium content in zebrafish brain tissue, leading to progressive impaired neurodevelopmental behaviours and latent learning and memory performance. Additionally, oxidative stress and disruption of dopaminergic transmission in zebrafish brain tissues are correlated with the dose-dependent and age-dependent accumulation of aluminium content. Moreover, the number of neural cells in the telencephalon tissue treated with Al₂O₃-NPs significantly declined, and the ultramicroscopic morphology indicated profound autophagy alternations. The results suggest that Al₂O₃-NPs has dose-dependent and time-dependent progressive damage on learning and memory performance in adult zebrafish when treated in embryos. This is the first study of the effects of Al₂O₃-NPs on learning and memory during the development of zebrafish from embryo to adult.

Keywords: Al(2)O(3) nanoparticles; Learning and memory; Neuroethology; Neurotransmitters; Oxidative stress; Zebrafish.