Aroclor 1254 and BDE-47 inhibit dopaminergic function manifesting as changes in locomotion behaviors in zebrafish embryos.

Contamination with polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in the environment is a major concern due to their persistent bioaccumulative toxicity that can disturb neurobehavioral functions including movements. Recently, it was reported that some PBDE including BDE-47 stimulates locomotor activities of zebrafish embryos by unknown mechanism. In this study, motor movements of the zebrafish embryo were used as a model system to evaluate the neuronal toxicity of a non-coplanar PCB-dominant mixture (Aroclor 1254) and BDE-47. Both organohalogens increased tail shaking and rotation of embryos in a concentration-dependent manner. Chemical inhibition and gene knock-down of tyrosine hydroxylase and vesicular monoamine transporter 2 (VMAT2) also induced hyperactivities. Hyperactivities induced by these treatments were all inhibited by supplementation of l-tyrosine and l-dopa, precursors of dopamine synthesis. Both organohalogens reduced dopamine contents and increased the 3,4-dihydroxyphenylacetic acid (DOPAC)/dopamine ratio in whole embryos. The results suggest that functional inhibition of dopaminergic neurons is involved in hyperactivities of zebrafish embryos caused by Aroclor 1254 and BDE-47.