ADVERTISEMENT
2 /3 FREE ARTICLES LEFT THIS MONTH Remaining
Chemistry matters. Join us to get the news you need.

If you have an ACS member number, please enter it here so we can link this account to your membership. (optional)

ACS values your privacy. By submitting your information, you are gaining access to C&EN and subscribing to our weekly newsletter. We use the information you provide to make your reading experience better, and we will never sell your data to third party members.

ENJOY UNLIMITED ACCES TO C&EN

Biological Chemistry

Immune Cells Trigger Pain

Blocking receptors could stop an immune system molecule that contributes to debilitating pain stemming from past nerve damage

by Sophie L. Rovner
April 27, 2009 | APPEARED IN VOLUME 87, ISSUE 17

[+]Enlarge
Credit: Courtesy of Makoto Tsuda
Nerve damage converts spinal microglia from a resting state (blue) to an activated state (orange) that elicits neuropathic pain.
8717scon2.gif
Credit: Courtesy of Makoto Tsuda
Nerve damage converts spinal microglia from a resting state (blue) to an activated state (orange) that elicits neuropathic pain.

Bouts of neuropathic pain stemming from nerve damage can be provoked by normally innocuous sensations such as the touch of clothing on the skin. Japanese researchers now report that an immune system molecule contributes to the development of this type of sometimes debilitating pain, for which there is no current treatment (Proc. Natl. Acad. Sci. USA, DOI: 10.1073/pnas.0810420106). Kazuhide Inoue and colleagues at Kyushu University, in Fukuoka, knew from prior studies that the amount of the inflammatory cytokine IFN-γ in the spinal cord increases after a nerve injury. Their new findings show that IFN-γ binds to a receptor on spinal immune cells known as microglia, thereby activating the cells. The researchers believe IFN-γ prompts the cells to increase production of compounds including Lyn tyrosine kinase and the receptor P2X4R, which increases the release of substances such as brain-derived neurotrophic factor, a protein that normally protects neurons. These changes trigger the hyperexcitability of spinal neurons that leads to neuropathic pain. Inoue and coworkers suggest that blocking IFN-γ signaling in spinal microglia could diminish neuropathic pain while leaving intact the normal pain-signaling pathways that alert a person to a harmful stimulus, such as a hot iron.

X

Article:

This article has been sent to the following recipient:

Leave A Comment

*Required to comment