Sensory plasticity caused by up-down regulation encodes the information of short-term learning and memory.

Learning and memory are essential for animals' well-being and survival. The underlying mechanisms are a major task of neuroscience studies. In this study, we identified a circuit consisting of ASER, RIC, RIS, and AIY, is required for short-term salt chemotaxis learning (SCL) in C. elegans. ASER NaCl-sensation possesses are remodeled by salt/food-deprivation pared conditioning. RIC integrates the sensory information of NaCl and food availability. It excites ASER and inhibits AIY by tyramine/TYRA-2 and octopamine/OCTR-1 signaling pathways, respectively. By the salt conditioning, RIC NaCl calcium response to NaCl is depressed, thus, the RIC excitation of ASER and inhibition of AIY are suppressed. ASER excites RIS by FLP-14/FRPR-10 signaling. RIS inhibits ASER via PDF-2/PDFR-1 signaling in negative feedback. ASER sensory plasticity caused by RIC plasticity and RIS negative feedback are required for both learning and memory recall. Thus, the sensation plasticity encodes the information of the short-term SCL that facilitates animal adaptation to dynamic environments.