Satiety quiescence is a behavioral state defined as a lack of movement or feeding following satiation. ASI is important for worms to enter satiety quiescence. We found the nutrients directly activate ASI. The nutrient rich stimulus we use in the lab is Luria broth (LB) and we are working to identify the active component by testing individual components of LB. Feeding is stimulated or suppressed depending not only on metabolic needs but also on environmental cues. To understand how feeding is controlled by environmental cues, we treated worms with nutrients mixed with noxious stimuli such as a high concentration of NaCl (4 M). 1 We found that these noxious stimuli override the ASI activation by nutrients, suggesting feeding, a potential result after sensing nutrients via ASI, can be suppressed in the presence of noxious stimuli. Furthermore, ASI suppression by noxious stimuli is entirely dependent on ASH function, a pair of neurons required for sensation of noxious stimuli. In an ASH genetic ablation background, ASI continue to respond to LB in the presence or absence of noxious stimuli. We believe there is a circuit between ASH, ASI, and an interneuron pair, AIA, which regulates ASI activation to nutrients. Our behavioral data show in an AIA genetic ablation background and an ASH genetic ablation background that satiety quiescence is enhanced when compared to concurrent controls, suggesting the signals from these neuron pairs inhibit ASI and satiety quiescence when they are intact. Recent work by others has identified a potential circuit between ASH and ASI that included three other neuron pairs RIM/RIC and ADF, although this circuit was not tested in the context of feeding or nutrient availability. 21. Chatzigeorgiou M, Bang S, Hwang SW, Schafer WR. tmc-1
encodes a sodium-sensitive channel required for salt chemosensation in C. elegans. Nature. 2013;494(7435):95-9. doi:10.1038/nature11845.2. Guo M, Wu T-H, Song Y-X, et al. Reciprocal inhibition between sensory ASH and ASI neurons modulates nociception and avoidance in Caenorhabditis elegans. Nat Commun. 2015;6:1-13. doi:10.1038/ncomms6655.