Abstract
Activated microglial cells generate reactive oxygen species (ROS), which have detrimental effects in neuroinflammatory and neurodegenerative diseases. In the present study, we have identified a novel mechanism involved in microglial NADPH oxidase-mediated ROS production. In PMA-stimulated microglia, ROS production was substantially reduced upon inhibition of the non-selective cation channel TRPV1 with La(3+), ruthenium red, capsazepine and 5-iodo-resinferatoxin. Furthermore, sustained membrane depolarization, a hallmark of NADPH oxidase activity in phagocytes, was found to induce non-selective cation/TRPV1 channel activity in microglia. Together, our data suggest that TRPV1 channels are involved in regulating NADPH oxidase-mediated ROS generation in microglia.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Capsaicin / analogs & derivatives
-
Capsaicin / pharmacology
-
Cell Line
-
Cell Respiration / drug effects
-
Cell Respiration / physiology
-
Diterpenes / pharmacology
-
Encephalitis / immunology
-
Encephalitis / metabolism*
-
Encephalitis / physiopathology
-
Gliosis / immunology
-
Gliosis / metabolism*
-
Gliosis / physiopathology
-
Ion Channel Gating / drug effects
-
Ion Channel Gating / physiology
-
Lanthanum / pharmacology
-
Membrane Potentials / drug effects
-
Membrane Potentials / physiology
-
Mice
-
Microglia / immunology
-
Microglia / metabolism*
-
NADPH Oxidases / metabolism
-
Organ Culture Techniques
-
Oxidative Stress / immunology*
-
Reactive Oxygen Species / metabolism*
-
Respiratory Burst / drug effects
-
Respiratory Burst / physiology
-
Ruthenium Red / pharmacology
-
TRPV Cation Channels / metabolism*
Substances
-
Diterpenes
-
Reactive Oxygen Species
-
TRPV Cation Channels
-
TRPV1 protein, mouse
-
Ruthenium Red
-
Lanthanum
-
resiniferatoxin
-
NADPH Oxidases
-
capsazepine
-
Capsaicin