Minocycline inhibits the enhancement of antidromic primary afferent stimulation-evoked vasodilation following intradermal capsaicin injection

@article{Gong2010MinocyclineIT,
  title={Minocycline inhibits the enhancement of antidromic primary afferent stimulation-evoked vasodilation following intradermal capsaicin injection},
  author={Kerui Gong and Yue Yue and Xiaoju Zou and Dingge Li and Qing Lin},
  journal={Neuroscience Letters},
  year={2010},
  volume={482},
  pages={177-181}
}

Figures from this paper

Intrathecal injection of fluorocitric acid inhibits the activation of glial cells causing reduced mirror pain in rats

Fluorocitrate can inhibit the activation of glial cells in spinal cord and DRG, and reduce MIP.

Sumatriptan improves the locomotor activity and neuropathic pain by modulating neuroinflammation in rat model of spinal cord injury

Sumatriptan improves functional recovery from SCI through its anti-inflammatory effects and reducing pro-inflammatory and pain mediators.

Spinal Glial Adaptations Occur in a Minimally Invasive Mouse Model of Endometriosis: Potential Implications for Lesion Etiology and Persistent Pelvic Pain

This is the first study to describe adaptations in nonneuronal, immune-like cells of the central nervous system attributed to the presence of endometriosis-like lesions, and spinal levels showing the greatest alterations in GFAP immunoreactivity appeared to correlate with the spatial location of lesions within the abdominopelvic cavity.

Minocycline inhibits neurogenic inflammation by blocking the effects of tumor necrosis factor‐α

It is proposed that minocycline is a potential therapeutic drug that can reduce neuronal excitability and neurogenic inflammation by working on SGCs to inhibit the expression of TNF‐α.

Minocycline as a promising therapeutic strategy for chronic pain.

References

SHOWING 1-10 OF 52 REFERENCES

Adelta and C primary afferents convey dorsal root reflexes after intradermal injection of capsaicin in rats.

The hypothesis that centrally mediated antidromic activity in Adelta and C primary afferent fibers contributes to the development of neurogenic inflammation, presumably by release of inflammatory substances in the periphery is supported.

Dorsal root reflexes and cutaneous neurogenic inflammation after intradermal injection of capsaicin in rats.

It is concluded that peripheral cutaneous inflammation induced by intradermal injection of capsaicin involves central nervous mechanisms and DRRs play a major role in the development of neurogenic Cutaneous inflammation, although a direct action of CAP on peripheral nerve terminals or the generation of axon reflexes also may contribute to changes in the skin near the injection site.

Roles of TRPV1 and neuropeptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin

The data suggest that the generation of DRRs is critical for driving the release of neuropeptides antidromically from primary afferent nociceptors following intradermal capsaicin injection and the released CGRP and SP participate in neurogenic inflammation.

Cellular Mechanisms of Neurogenic Inflammation

The challenge remains to ascertain the critical transduction pathways that regulate transmitter release from sensory neurons since this phenomenon triggers neurogenic inflammation, and the cellular mechanisms involved in alterations in neuronal excitability during injury and the Cellular pathways that maintain the inflammatory response over time need to be determined.

Intrathecal minocycline attenuates peripheral inflammation‐induced hyperalgesia by inhibiting p38 MAPK in spinal microglia

Findings show that minocycline given IT produces a potent and consistent antinociception in models of tissue injury and inflammation‐evoked pain, and they provide strong support for the idea that this effect is mediated by direct inhibition of spinal microglia and subsequent activation of p38 in these cells.
...