By Nicole Tay
One thing I’ve learned about living in Boston is that the mosquitoes here are vicious. They fly around almost silently, and by the time you notice them, it’s too late; they’ve already made a snack of you.
In one particular case, I was driving home from work and noticed I had an unwelcome passenger. The commute turned into an anxiety-ridden nightmare: lots of swatting while driving and many awkward attempts to lure her out the window. This would not end well, I knew. Sure enough, when I got home, I had bites everywhere. (Apparently, Boston mosquitoes can bite you through tights?!)
The itching comes next. Everyone knows not to scratch bites and itches, but few of us have the superhuman self-discipline to resist the urge. I had even deluded myself into pseudo-scientifically justifying my scratching: “If scratching relieves itchiness, it’s obviously due to some beneficial neuronal pathway, right?”
Wrong. New research from Washington University School of Medicine in St. Louis says otherwise: Scratching can relieve itch by creating minor pain. But when the body responds to pain signals, that response actually can make itching worse.
In essence, when we scratch, the resulting pain interferes with the itchiness and the brain releases serotonin to quell that pain. The serotonin then binds to certain receptors on certain neurons that stimulate the itchy sensation. From the press release:
As part of the study, the researchers bred a strain of mice that lacked the genes to make serotonin. When those genetically engineered mice were injected with a substance that normally makes the skin itch, the mice didn’t scratch as much as their normal littermates. But when the genetically altered mice were injected with serotonin, they scratched as mice would be expected to in response to compounds designed to induce itching.
[To identify the specific serotonin receptor, senior investigator Zhou-Feng] Chen’s team injected mice with a substance that causes itching. They also gave the mice compounds that activated various serotonin receptors on nerve cells. Ultimately, they learned that the receptor known as 5HT1A was the key to activating the itch-specific GRPR neurons in the spinal cord.
To prove they had the correct receptor, Chen’s team also treated mice with a compound that blocked the 5HT1A receptor, and those mice scratched much less. Continue reading