Premium
Kainate induces rapid redistribution of the actin cytoskeleton in ameboid microglia
Author(s) -
Christensen Randolph N.,
Ha Byeong Keun,
Sun Fang,
Bresnahan Jacqueline C.,
Beattie Michael S.
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20865
Subject(s) - kainate receptor , glutamate receptor , microglia , microbiology and biotechnology , biology , membrane ruffling , phalloidin , ampa receptor , neurotransmitter receptor , cytoskeleton , neuroscience , receptor , immunology , biochemistry , inflammation , cell
Abstract Microglia are key mediators of the immune response in the central nervous system (CNS). They are closely related to macrophages and undergo dramatic morphological and functional changes after CNS trauma or excitotoxic lesions. Microglia can be directly stimulated by excitatory neurotransmitters and are known to express many neurotransmitter receptors. The role of these receptors, however, is not clear. This study describes the microglial response to the glutamate receptor agonist kainate (KA) and shows via immunochemistry that the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionate (AMPA)‐type glutamate receptor subunit GluR1 is present on cultured microglia. In the presence of 100 μM or 1 mM KA, cultured microglia underwent dramatic morphological and cytoskeletal changes as observed by time‐lapse photography and quantitative confocal analysis of phalloidin labeling. KA‐stimulated microglia showed condensation of cytoplasmic actin filaments, rapid de‐ and repolymerization, and cytoplasmic redistribution of condensed actin bundles. Rearrangement of actin filaments—thought to be involved in locomotion and phagocytosis and to indicate an increased level of activation (for reviews see Greenberg [ 1995] Trends Cell Biol. 5:93–99; Imai and Kohsaka [ 2002] Glia 40:164–174)—was significantly increased in treated vs. control cultures. Morphological plasticity and membrane ruffling were also seen. These findings suggest direct microglial excitation via glutamate receptor pathways. Thus, neurotransmitter release after brain or spinal cord injury might directly modulate the inflammatory response. © 2006 Wiley‐Liss, Inc.