[
International Worm Meeting,
2021]
Neurons adapt to sensory experience through mechanisms that couple neural activity to gene expression changes. To what extent this mechanism alters behavioral programs, and how activity-dependent changes are coordinated across a neural circuit, is unclear. In C. elegans prolonged exposure to low oxygen (O2) levels reprograms O2-escape behavior, sculpts responses to other sensory cues and alters stimulus-evoked Ca2+ responses. To characterize the molecular changes that underpin this plasticity, we use cell-type-specific RNA sequencing to profile separate components of the O2-circuit in animals grown at either high (21%) or low (7%) O2. In each profiled component, we identify hundreds of experience-regulated genes, including neuropeptides, neuropeptide receptors, transcription factors and gap junctions. We show that experience-dependent regulation of these genes is contingent on O2-evoked activity within the O2-circuit. Across the circuit, transcriptional programs initiated by low O2 are mostly different between O2-sensing neurons and downstream interneurons. Despite these differences, we identify a large number of neuropeptide genes that show activity-regulated gene expression in both neural classes including short uncharacterised peptides which are likely to be secreted. Blocking peptidergic signalling from the RMG interneurons prevents animals to fully reprogram their O2-escape behavior. By comparison, blocking synaptic communication or peptidergic signalling in O2-sensing neurons has relatively little effect on the experience-dependent plasticity of O2-responses. These findings suggest a model where information about O2 experience is broadcasted from interneurons using neuropeptides to reprogram downstream circuits and behavior. This mechanism could help shed light on how activity-dependent changes are coordinated across neural circuits.