Microglia, the resident macrophages of the central nervous system (CNS
), are activated rapidly in response to neuronal injury. In the search
for factors which regulate inflammation resulting from pathology in t
he CNS, it is logical to focus on changes in the local environment whi
ch occur following neuronal death. These include transient alterations
in transmembrane ion gradients. Electrophysiological studies have pro
vided information on the range of ion channels expressed by macrophage
s and microglia in vitro. The purpose of this study was to focus on th
e biology of macrophages and the role ion channels play in determining
their activity. We show that potassium channels are unlikely to be in
volved in the generation of nitric oxide by activated macrophages and
microglial cell lines in vitro. Chloride channels are more likely to c
ontribute to this response. Our results question the functional import
ance of the observed differences between the channel expression in vit
ro of macrophages and microglia. (C) 1998 Wiley-Liss, Inc.