Possible different mechanism between amyloid-beta (25-35)-and substance P-induced chemotaxis of murine microglia.

The mechanism of murine microglial chemotaxis induced by amyloid-beta protein (A beta (25-35)) was investigated. A beta (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 A beta (25-35). The chemotactic effect of microglia was homologously desensitized by 10 nM A beta (25-35). On the other hand, substance P at 10 nM did not desensitize the A beta (25-35)-induced chemotaxis. These data show that A beta (25-35) induces the chemotaxis of microglia probably through a receptor other than the NK-1 receptor.