Some nerve cells that make us itch also make us feel pain, finds study.



London, May 3 (ANI): A new study has found growing evidence that nerve cells that make us itch can also make us feel pain.

Itch and pain researcher Diana Bautista, an assistant professor of molecular and cell biology at the University of California, Berkeley, said that the interactions between itch and pain are only partly understood.

The skin contains some nerve cells that respond only to itch and others that respond only to pain. Others, however, respond to both, and some substances cause both itching and pain.

Bautista's new research shows that two specific irritants induce itching by way of the wasabi receptor, a pain receptor familiar to sushi lovers.

Other recent studies have shown that some itch inducers, called pruritogens, lead to activation of the capsaicin receptor, a pain receptor named for the incendiary chemical in chili peppers.

"It's starting to look like many pain receptors are linked to the itch system. Both itch and pain use some of the same molecules to send signals to the brain," she said.

Bautista has genetically altered mice so that they don't produce the wasabi receptor, and hopes that the mouse strain will help lead to a better understanding of forms of itch that do not respond to antihistamines.

Five years ago, Bautista showed that allyl isothiocyanate, the sinus-clearing ingredient in wasabi, hot mustard and garlic, causes pain solely by activating a receptor called TRPA1 on sensory nerves.

The receptor is one of a group of transient receptor potential (TRP) ion channels in sensory nerves under the skin, including the mouth and mucus membranes, which detect temperature, mechanical abrasion and irritating chemicals.

The capsaicin and heat receptor, dubbed TRPV1, is another such ion channel, as is TRPM8, a cold-activated channel targeted by menthol and other cooling agents.

When these receptors are activated, they open up and depolarise the nerve cell, which transmits an attention-grabbing pain signal through the spinal cord to the brain.

Bautista's colleague Xinzhong Dong in the Solomon H. Snyder Department of Neuroscience at Johns Hopkins University School of Medicine in Baltimore recently identified two new itch receptors, both of them Mas-related G protein-coupled receptors.

One, MrgprA3, is stimulated by chloroquine, while the second, MrgprC11, is stimulated by BAM8-22, a peptide released by immune cells, including mast cells, during inflammation.

If sensory nerves contain pain receptors like TRPA1 and TRPV1, and itch receptors like MrgprA3 and MrgprC11, how does the cell distinguish between itch and pain? Bautista asked.

Bautista tested both chloroquine and the mast cell chemical BAM8-22 on cultured mouse cells and found that both activate the wasabi receptor, TRPA1, causing a depolarisation of nerve cells.

In addition, knock-out mice that lack the receptor do not respond to either chemical, while a chemical that blocks the receptor also stops the itch.

Her interpretation of the results is that in sensory nerves with both the chloroquine itch receptor and the wasabi pain receptor, when chloroquine binds to its receptor, it subsequently opens the wasabi receptor, which depolarises the nerve cell and sends an itch signal to the brain.

Similarly, in the cells that have both a BAM8-22 itch receptor and a wasabi receptor, BAM8-22 triggers opening of the wasabi receptor. Both itch inducers trigger the pain receptors through G protein couplings inside the cell.

"These experiments provide a wonderful demonstration that chloroquine and BAM8-22 cause itch only through the wasabi receptor," she said.

"If both pathways converge on the same ion channel, perhaps other molecules that cause itch also use this channel," she added.

The findings have been published in this week's print edition of the journal Nature Neuroscience. (ANI)

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