The ability to sense and respond to pain is critical for avoiding bodily harm. Chronic pain, however, is a debilitating condition that affects more than 25 million adults in the US. A mechanistic understanding of the neural basis of pain is needed to develop better therapies to treat pain. The parabrachial nucleus (PBN) is a hindbrain structure that integrates peripheral information, including pain, and transmits these signals throughout the brain. Our prior work suggests that Neuropeptide Y (NPY) plays a role in signaling pain behavior by binding to the NPY-Y1 receptor in the PBN. Based on this research, we hypothesized that NPY-Y1 receptor- expressing neurons in the PBN are activated by painful stimuli. To test this hypothesis, we used fiber photometry in mice to measure in vivo calcium dynamics as a proxy for neural activity in awake, behaving animals. We administered a 2% formalin injection in the dorsal hindpaw which causes acute pain followed by a distinct, longer-term inflammatory phase. Mice respond to pain by licking the affected paw, allowing us to use the time spent licking the injected paw as a behavioral readout of pain. We simultaneously measured the activity levels of NPY-Y1 receptor-expressing neurons. We found that heightened neural activity of the NPY-Y1 receptor-expressing neurons correlated with pain in both the acute and inflammatory phases. Our results support our hypothesis that NPY-Y1 receptor- expressing neurons are involved in pain signaling. To test the functional relationship between this neural population and pain behavior we will inactivate NPY-Y1 receptor-expressing neurons using chemo or optogenetics. We expect that inactivating NPY-Y1 receptor-expressing neurons will attenuate paw licking, further supporting our hypothesis that this neural population plays an important role in pain processing.