Affiliations: Keck School of Medicine, University of Southern California, Los Angeles, CA, USA | CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal | Health Sciences Research Center, University of Beira Interior, Covilhã, Portugal
Note: [] Correspondence to: Dr. Raquel Ferreira, Keck School of Medicine, University of Southern California, Health Science Campus, 2011 Zonal Avenue, HMR 315, 90033 Los Angeles, CA, USA. Tel.: +1 323 442 1150; Fax: +1 323 442 3049; E-mails: raquelmargarida@gmail.com, tiagodesousasantos@gmail.com (T. Santos); libernardino@gmail.com (L. Bernardino).
Abstract: Microglia are the smallest member of the glia family but greatly responsible for vital physiological responses to brain injury and/or infection. The resulting inflammatory process includes the recruitment of microglial cells to the site of injury, the release of both toxic and trophic molecules and the clearance of invading pathogens or dead cells. The purpose of this review is to detail the role of neuropeptide Y (NPY) over microglia principal activities. In addition, we also summarize the main effects of other neuropeptides, such as galanin, somatostatin, substance P, pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP). Recently, we showed that NPY downregulates the innate immune response, by decreasing the release of interleukin-1β and nitric oxide, migration and phagocytosis by activated microglia cells. A huge body of evidence has also showed that the reduction of microglia inflammatory responses supports regenerative mechanisms aiming at the protection of susceptible neurons in several brain diseases. Therefore, the neuroprotective and immunosuppressive effects of NPY in microglia cells suggest that it can be a key therapeutic target against Central Nervous System injury or disease.
Keywords: Neuropeptide Y, microglia, inflammation, migration, phagocytosis, cytokines
