Transmissions of serotonin, dopamine, and glutamate are required for the formation of neurotoxicity from Al₂O₃-NPs in nematode Caenorhabditis elegans

Abstract

In this study, we investigated genetic mechanisms of neurotransmitters in regulating the formation of adverse effects on locomotion behavior in Al₂O₃ nanoparticles (NPs)-exposed Caenorhabditis elegans. Al₂O₃-NPs exposure caused the decrease of locomotion behavior with head thrash and body bend as endpoints. Interestingly, the neurotransmitters of glutamate, serotonin, and dopamine were required for the adverse effects of Al₂O₃-NPs on locomotion behavior in nematodes. Glutamate transporter EAT-4, serotonin transporter MOD-5, and dopamine transporter DAT-1 might serve as the molecular targets of Al₂O₃-NPs for neurotoxicity formation. Moreover, the behavioral response of nematodes to Al₂O₃-NPs exposure was primarily mediated by non-NMDA glutamate receptors GLR-2 and GLR-6, ionotropic serotonin receptor MOD-1, and D1-like dopamine receptor DOP-1. Therefore, Al₂O₃-NPs exposure influences locomotion behavior of nematodes primarily by impinging on their glutamatergic, serotoninergic, and dopaminergic systems. Our data will shed light on questions surrounding the involvement of neurotransmitters in mediating the adverse behavioral effects from Al₂O₃-NPs.

Keywords::

• Nanotoxicology
• Caenorhabditis elegans
• Al₂O₃ nanoparticle
• neurotransmitter
• neurotoxicology

Acknowledgements

The nematode strains used were provided by the Caenorhabditis Genetics Center (funded by the NIH National Center for Research Resource, USA). This work was supported by grants from the National Basic Research Program of China (No. 2011CB933404), the National Natural Science Foundation of China (No. 81172698), and the Postdoctoral Foundation of China (2011M500835).