You are viewing a javascript disabled version of the site. Please enable Javascript for this site to function properly.
Go to headerGo to navigationGo to searchGo to contentsGo to footer
In content section. Select this link to jump to navigation

Neuropeptides as Attractants of Immune Cells in the Brain and their Distinct Signaling

Article type: Research Article

Authors: Noda, Mami | Ifuku, Masataka | Okuno, Yuko | Beppu, Kaoru | Mori, Yuki | Naoe, Satoko

Affiliations: Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan

Note: [] Correspondence to: Mami Noda, Ph.D., Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan. 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Tel./Fax: +81 92 642 6574; E-mail: [email protected]

Keywords: Microglia, migration, ATP, neuropeptides, Ca\(^{\rm{2+}}\)-dependent K\(^{\rm{+}}\) channels, Na\(^{\rm{+}}\)/Ca\(^{\rm{2+}}\) exchange mechanism, IP\(_{\rm{3}}\)

DOI: 10.3233/NIB-2011-005

Journal: Advances in Neuroimmune Biology, vol. 1, no. 1, pp. 53-62, 2011

Published: 2011
Get PDF open access

Abstract

Microglia, the immune cells of the central nervous system (CNS), are busy and vigilant housekeepers in the adult brain. The main candidate as a chemoattractant for microglia at damaged site is adenosine triphosphate (ATP). However, many other substances can induce immediate change of microglia. Some neuropeptides such as angiotensin II, bradykinin (BK), endothelin, galanin (GAL), and neurotensin are also chemoattractants for microglia. Among them, BK increased microglial migration via B1 receptor with different mechanism from that of ATP. BK-induced migration was controlled by a Gi/o protein-independent pathway, while ATP-induced migration was via a Gi/o protein-dependent and also a mitogen-activated protein kinase (MAPK) / extracellular signal-regulated kinase (ERK)-dependent pathway. On the other hand, GAL is reported to have a similar signal cascade as that of BK, though only part of the signaling was similar to that of BK-induced migration. For example, BK activates reverse-mode Na+/Ca2+ exchange allowing extracllular Ca2+ influx, while GAL induces intracellular Ca2+ mobilization via increasing inositol-1,4,5-trisphosphate. In addition, GAL activates MAPK/ERK-dependent signaling but BK did not. These results suggest that chemoattractants for immune cells in the brain including ATP and each peptide may have distinct role under both physiological and pathophysiological conditions.

Show less