| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6265248 | Brain Research | 2011 | 9 Pages |
Minocycline is an inhibitor of microglial activation and proliferation. Minocycline suppresses pain-related behaviors in many different pain states, which correlates closely with its inhibition of microglial activation and subsequent release of pro-inflammatory mediators in the spinal cord. Na+ channels in dorsal root ganglion (DRG) neurons are implicated in the generation of inflammatory and neuropathic pain. To elucidate a possible peripheral mechanism of minocycline analgesia, effects of minocycline on tetrodotoxin-sensitive and tetrodotoxin-resistant Na+ currents in rat DRG neurons were investigated. Minocycline potently inhibited both types of Na+ currents with IC50 values of 350Â nM and 410Â nM, respectively. The inhibition was accompanied by a depolarizing shift of the activation voltage. However, minocycline slowed the inactivation and speeded up the recovery from inactivation. These results suggest minocycline may exert analgesia peripherally thorough Na+ channel inhibition in the primary afferent neurons as well as centrally through microglial inhibition in the spinal cord.
Research HighlightsâºMinocycline inhibits Na+ currents in rat dorsal root ganglion neurons. âºMinocycline produces a depolarizing shift in the activation voltage of Na+ currents. âºMinocycline slows the inactivation of Na+ currents. âºMinocycline speeds up the recovery of Na+ currents from inactivation. âºInhibition of Na+ currents is considered as an analgesic mechanism of minocycline.
