Contribution of the central amygdala-zona incerta pathway in the modulation of persistent pathological pain
Thursday, September 14, 2017 — Poster Session III
- LS Valdivia Torres
- D Velasquez
- S Arango
- T Wilson
- Y Carrasquillo
The central amygdala (CeA) has been identified as a neural center for the modulation of pain. Cells expressing protein kinase C d (PKCd) are one of the predominant population of CeA cells (CeA-PKCd). Results from ongoing experiments in our lab demonstrate that activity of CeA-PKCd cells is necessary for the modulation of tactile hypersensitivity in a mouse model of persistent pain. The anatomical circuitry underlying the modulation of pain-related behaviors by CeA-PKCd cells, however, remains unknown. To begin to address this question, we performed a thorough analysis of the efferent projections of CeA-PKCd neurons within the entire mouse brain, using a viral-vector-mediated cell-type-specific anterograde tracing. One of the regions identified in these anatomical experiments was the zona incerta (ZI), a subthalamic nucleus that has been previously suggested to contribute to the modulation of visceral activity, arousal, posture and locomotion and pain-related behaviors. Based on the previous studies showing modulation of pain-related behaviors in the ZI and our anatomical findings identifying the ZI as an efferent target of CeA-PKCd cells, we hypothesized that modulation of pain-related behaviors by CeA-PKCd cells is mediated via downstream modulation of the ZI. We have already confirmed that CeA-PKCd cells project to the ZI by injecting a retrograde tracer into the ZI of PKCd-cre::Ai9 mice and quantifying the CeA cells that take up the tracer and are PKCd+. Ongoing experiments aim at using in-vivo optogenetics in combination with mouse behavioral approaches to evaluate the physiological contribution of the CeA-ZI pathway to the modulation of pain-related behaviors.