| First Author | Moritz C | Year | 2015 |
| Journal | Neurosci Lett | Volume | 591 |
| Pages | 13-8 | PubMed ID | 25666889 |
| Mgi Jnum | J:219951 | Mgi Id | MGI:5630016 |
| Doi | 10.1016/j.neulet.2015.02.004 | Citation | Moritz C, et al. (2015) Live imaging reveals a new role for the sigma-1 (sigma1) receptor in allowing microglia to leave brain injuries. Neurosci Lett 591:13-8 |
| abstractText | Microglial cells are responsible for clearing and maintaining the central nervous system (CNS) microenvironment. Upon brain damage, they move toward injuries to clear the area by engulfing dying neurons. However, in the context of many neurological disorders chronic microglial responses are responsible for neurodegeneration. Therefore, it is important to understand how these cells can be "switched-off" and regain their ramified state. Current research suggests that microglial inflammatory responses can be inhibited by sigma (sigma) receptor activation. Here, we take advantage of the optical transparency of the zebrafish embryo to study the role of sigma1 receptor in microglia in an intact living brain. By combining chemical approaches with real time imaging we found that treatment with PB190, a sigma1 agonist, blocks microglial migration toward injuries leaving cellular baseline motility and the engulfment of apoptotic neurons unaffected. Most importantly, by taking a reverse genetic approach, we discovered that the role of sigma1in vivo is to "switch-off" microglia after they responded to an injury allowing for these cells to leave the site of damage. This indicates that pharmacological manipulation of sigma1 receptor modulates microglial responses providing new approaches to reduce the devastating impact that microglia have in neurodegenerative diseases. |
