Dietary restriction (DR), a non-genetic, non-pharmacological treatment, represents one of the most effective means to promote longevity in all tested animal models, ranging from worms to mammals. However, the underlying mechanisms remain incompletely understood. Besides nutrients, non-nutrient food components, such as food odors, also regulate longevity. For example, food odors suppress DR-mediated longevity by regulating the sensitivity of the chemosensory neuron ADF to food odors in C. elegans, a widely employed genetic model for aging research. How DR regulates the odor sensitivity of ADF neurons, however, remains unclear. It is also unclear whether DR regulates the odor sensitivity of other chemosensory neurons in C. elegans and if so, whether such regulation contributes to DR-mediated longevity. Here, by screening all the chemosensory neurons in C. elegans, we show that in addition to ADF, several chemosensory neurons, such as ASI and BAG, are also sensitive to food odors and that their odor sensitivity is regulated by DR. Ablating ASI neurons shortens DR-mediated longevity, demonstrating that these chemosensory neurons contribute to DR-mediated longevity. We further show that DR regulates the odor sensitivity of ADF neuron through mTORC1-FOXO signaling, which up-regulates genes crucial for chemosensory transduction, such as those encoding the chemosensory receptor SRB-16 and the TRP ion channel OSM-9, leading to enhanced odor sensitivity in ADF. These results advance our understanding of how food odors regulate DR longevity through chemosensory neurons and how DR regulates the function of these neurons.