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Updated: Aug 13, 2026
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Published on: April 11, 2018
Systemic administration of minocycline inhibits formalin-induced inflammatory pain in rat
Ik-Hyun Cho1, Young Min Chung, Chul-Kyu Park
1Department of Physiology and Program in Molecular and Cellular Neuroscience, Seoul National University, 28-2 Yeongeon-Dong Chongno-Ku, Seoul 110-749, Korea.
Abstract:
It has been demonstrated that spinal microglial activation is involved in formalin-induced pain and that minocycline, an inhibitor of microglial activation, attenuate behavioral hypersensitivity in neuropathic pain models. We investigated whether minocycline could have any anti-nociceptive effect on inflammatory pain, after intraperitonial administration of minocycline, 1 h before formalin (5%, 50 microl) injection into the plantar surface of rat hindpaw. Minocycline (15, 30, and 45 mg/kg) significantly decreased formalin-induced nociceptive behavior during phase II, but not during phase I. The enhancement in the number of c-Fos-positive cells in the L4-5 spinal dorsal horn (DH) and the magnitude of paw edema induced by formalin injection during phase II were significantly reduced by minocycline. Minocycline inhibited synaptic currents of substantia gelatinosa (SG) neurons in the spinal DH, whereas membrane electrical properties of dorsal root ganglion neurons were not affected by minocycline. Analysis with OX-42 antibody revealed the inhibitory effect of minocycline on microglial activation 3 days after formalin injection. These results demonstrate the anti-nociceptive effect of minocycline on formalin-induced inflammatory pain. In addition to the well-known inhibitory action of minocycline on microglial activation, the anti-edematous action in peripheral tissue, as well as the inhibition of synaptic transmission in SG neurons, is likely to be associated with the anti-nociceptive effect of minocycline.
Insights
Minocycline reduces inflammatory pain by inhibiting spinal microglial activation and synaptic transmission. This study shows minocycline
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Spinal microglial activation contributes to inflammatory pain.
- Minocycline inhibits microglial activation and shows efficacy in neuropathic pain models.
Purpose of the Study:
- To investigate the anti-nociceptive effect of minocycline on formalin-induced inflammatory pain.
- To explore the mechanisms underlying minocycline's action.
Main Methods:
- Minocycline was administered intraperitoneally to rats before formalin injection.
- Nociceptive behavior, paw edema, c-Fos expression, and synaptic currents were measured.
- Microglial activation was assessed using OX-42 antibody.
Main Results:
- Minocycline significantly reduced nociceptive behavior during phase II of the formalin test.
- It decreased paw edema and the number of c-Fos-positive cells in the spinal dorsal horn.
- Minocycline inhibited synaptic currents in substantia gelatinosa neurons but did not affect dorsal root ganglion neurons.
Conclusions:
- Minocycline exhibits anti-nociceptive effects on formalin-induced inflammatory pain.
- Its actions are associated with inhibition of microglial activation, peripheral anti-edematous effects, and reduced synaptic transmission in the spinal cord.
