Sensory Plasticity Caused by Up-down Regulation Encodes the Information of Short-term Learning and Memory

Abstract

Learning and memory are essential for animals’ well-being and surviving. The underlying mechanisms are a major task of neuroscience studies. In this study, we identified a circuit consisting ASER, RIC, RIS, and AIY, required for short-term salt chemotaxis learning (SCL) in C. elegans. ASER NaCl sensation possesses ON- and OFF-responses and is remodeled by salt conditioning. RIC integrates sensory information of NaCl stimulation and food deprivation and generates a suppression of its NaCl calcium response by salt conditioning. RIC plasticity combining with interaction between ASER and RIS generates ASER sensory plasticity that is required for learning and memory recalling. We further identify the signaling pathways between neurons in the circuit: tyramine/TYRA-2 and octopamine/OCTR-1 signaling mediate neurohumoral regulation of AIY and ASER by RIC; FLP-14/FRPR-10 and PDF-2/PDFR-1 signalings mediate the transmission of humoral regulation from ASER to RIS and the feedback from RIS to ASER, respectively. Thus, ASER sensory plasticity encodes the information of the short-term SCL, which can facilitate animal adaptation to dynamic environments.