Monday, January 31, 2011

The "itch receptor"

Another thing for me to be excited about: this Thursday, I get to talk to Gil Yosipovitch, the "Godfather of Itch," who runs a clinic at Wake Forest University and founded the International Forum for the Study of Itch. (I made him an offer he couldn't refuse.) If you have any questions for him, please ask and I will pass them along. Myself, I just want to get an idea of how his clinic operates, and find out why there aren't more of them.

Also, whether he envisions any pharmaceutical cures for itch appearing soon. Martin Steinhoff scribbled a list of possible targets in the itch pathway that one might like to shut down to reduce or eliminate itch. Here's what he wrote down, before I distracted him with another question:
  • GABA
  • GRP
  • Proteases
The "GRP" rang a bell in my memory so I looked it up. It stands for "gastrin-releasing peptide," whatever that is. What's important is that in 2007, two scientists at Washington University in St. Louis discovered that a receptor for GRP is a major gate for itch nerve impulses in the spinal cord, at least in mice. (And basic neurology isn't different in mice and humans.) I could be wrong, but I think that GRP receptor is still the prime suspect.

The scientists were able to do their experiments because they had developed a strain of mice without GRP receptors. These mice were much less likely to scratch themselves when their skin was injected with substances known to induce itch. And in normal mice, a compound that inhibits GRP receptors greatly reduced scratching behavior.

This isn't exactly breaking news, but it is good for me to know as I explore "itch centers" in the US and around the world.
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A wee  bit of business news: a small company in Seattle, recently acquired by Bristol-Myers Squibb, is developing an anti-IL-31 antibody which is now in preclinical trials for atopic dermatitis. (Now, what does IL-31 do? I always get confused by these IL-X things. It is apparently produced by Th2 cells and has something to do with inflammation.

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