Possible Different Mechanism between Amyloid-Beta (25–35)- and Substance P-lnduced Chemotaxis of Murine Microglia

Publisher Website
Google Scholar
Abstract
The mechanism of murine microglial chemotaxis induced by amyloid-β protein (Aβ(25–35)) was investigated. Aβ(25–35) dose-dependently stimulated microglial chemotaxis at concentrations between 100 pM and 10 nM. Substance P, a NK-1 agonist, stimulated chemotaxis at concentrations of 10 nM or more. GR-64349, a NK-2 agonist, and senktide, a NK-3 agonist, did not stimulate microglial chemotaxis. We examined whether homologous desensitization of chemotaxis would occur by Aβ(25–35). The chemotactic effect of microglia was homologously desensitized by 10 nM Aβ(25–35). On the other hand, substance P at 10 nM did not desensitize the Aβ(25–35)-induced chemotaxis. These data show that Aβ(25–35) induces the chemotaxis of microglia probably through a receptor other than the NK-1 receptor.

This publication has 0 references indexed in Scilit: