Possible different mechanism between amyloid-beta (25-35)-and substance P-induced chemotaxis of murine microglia - PubMed (original) (raw)
Comparative Study
doi: 10.1159/000213881.
Affiliations
- PMID: 9187934
- DOI: 10.1159/000213881
Comparative Study
Possible different mechanism between amyloid-beta (25-35)-and substance P-induced chemotaxis of murine microglia
K Maeda et al. Gerontology. 1997.
Abstract
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.
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