We also seek to define the cellular, circuit, and neuromodulatory organization of central amygdala (CeA) networks under baseline conditions and in models of acute and chronic pain. By integrating genetic tools, physiology, circuit mapping, and behavior, we examine how heterogeneous CeA neuron populations contribute to pain processing and how the bioactive lysosphingolipid  mediator, sphingosine‑1‑phosphate (S1P),  modulates their function. This approach establishes how lipid signaling and amygdala circuits are reconfigured in persistent pain states.