Abstract
Mechanosensitive channel (MSC) activity elicited by stretching membrane patches or by cell indentation is tightly coupled to the state of the cytoskeleton. To determine how stress in the cytoskeleton changes in the presence of inflammatory mediators we transiently expressed multiple cpstFRET probe chimeras (actinin, filamin and spectrin) in dorsal root ganglion (DRG) neurons and measured their stress responses in the indentation assay. PGE2 significantly increased both the resting stress and the stress response upon indentation in multiple cytoskeletal chimeras. PGE2 induced a robust increase in stress in filamin probes in the indentation assay. In the same assay, CGS-21680 induced a moderate increase in stress whereas 5-HT (serotonin) did not influence stress. The stress change profile resulting from the application of the above-mentioned inflammatory mediators (PGE2, CGS-21680 and 5-HT) correlated with the changes in endogenous mechanosensitive currents elicited by indenting DRG neurons. PGE2 increased mechanosensitive current substantially whereas only moderate increases were observed for CGS-21680 and 5-HT.
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