Preference choice on food is an important response strategy for animals living in the environment. Using assay system of preference choice on bacterial foods, OP50 and PA14, we identified the involvement of ADL sensory neurons in the control of preference choice in Caenorhabditis elegans. Both genetically silencing and ChR2-mediated activation of ADL sensory neurons significantly affected preference choice. ADL regulated preference choice by inhibiting function of G protein-coupled receptor (GPCR)/SRH-220. ADL sensory neurons might regulate preference choice through peptidergic signals of FLP-4 and NLP-10, and function of FLP-4 or NLP-10 in regulating preference choice was regulated by SRH-220. FLP-4 released from ADL sensory neurons further regulated preference choice through its receptor of NPR-4 in AIB interneurons. In AIB interneurons, NPR-4 was involved in the control of preference choice by activating the functions of ASH-2 trithorax complex consisting of SET-2, ASH-2, and WDR-5, implying the crucial role of molecular machinery of trimethylation of histone H3K4 in the preference choice control. The identified novel neuronal circuit and the underlying molecular mechanisms will strengthen our understanding neuronal basis of preference choice in animals.
We investigated the protective effects of vitamin E against the in vivo neurotoxicity of Al 2 O 3 -nanoparticles (NPs) in Caenorhabditis elegans. Al 2 O 3 -NPs in the range of mg L −1 led to neurodegeneration related phenotypes including neuronal loss, abnormality of axon development, and gap formation on nerve cords in the GABAergic nervous system and some behavioral deficits. Pretreatment with 200 mg L −1 of vitamin E prevented the neurotoxicity of Al 2 O 3 -NPs by reducing both the neurodegeneration and behavioral deficits. As for the underlying mechanism, pretreatment with vitamin E prevented the induction of oxidative stress, and sustained the normal intestinal permeability and development in Al 2 O 3 -NPs exposed animals. Moreover, pretreatment with vitamin E inhibited the translocation of Al 2 O 3 -NPs through the intestinal barrier into other parts of nematodes. Vitamin E-pretreated animals also showed less abnormality in the development of neurons involved in behavioral control and expression pattern of genes regulating cell identity of the corresponding neurons. Our results will be helpful for designing effective strategies to ameliorate nanotoxicity.
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