The Newsroom    Published Tuesday, Oct. 29, 2013, 9:08 AM
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Medical Discovery News - Where does itchiness come from?

Galveston County Daily News, October 29, 2013

By NORBERT HERZOG and DAVID NIESEL

Anyone ever bitten by a mosquito can attest to its itchy consequences.

New research has discovered just how our bodies detect and process itching, leading to a better understanding of our reaction to itching and hopefully better treatments for it.

The clinical term for an itch is “pruritus,” and at least 16 percent of people experience an itch that just doesn’t go away.

Long-term itching is the most common dermatologic complaint and can be caused by chronic renal disease, cirrhosis, some cancers, multiple sclerosis, diabetes, shingles, allergic reactions, drug reactions and pregnancy.

Prolonged itching and scratching can increase the intensity of the itch, possibly leading to neurodermatitis, a condition in which a frequently scratched area of skin becomes thick and leathery. The patches can be raw, red or darker than the rest of the skin.

Persistent scratching also can lead to a bacterial skin infection, permanent scars or changes in skin color. The strong pain reliever morphine can cause such a severe whole-body itch that some patients choose to forgo it and live with the pain.

Sensory neurons called TRPV1 cells detect itchy substances on skin. TRPV1 cells have long nerve fibers that extend into skin, muscle and other tissues to help monitor conditions.

It has not been clear how these neurons sort through different sensations like pain and temperature and route the signal along the proper pathway to the appropriate area of the brain for perception.

New research has revealed a small group of those neurons produce a substance called natriuretic polypeptide b (Nppb), a hormone known to be involved in regulating the heart.

Surprisingly, when Nppb is produced by TRPV1 cells it acts as a neurotransmitter, a chemical messenger secreted by neurons to carry, boost and control signals between neurons and other cells.

When scientists genetically modified mice to eliminate Nppb, they did not itch. Nppb binds to a specific receptor called Npra on particular nerves in the spinal column.

When those cells were eliminated in mice, again, they did not itch. Interestingly, removing these cells did not impact other sensory sensations such as temperature, pain and touch.

A similar transmission presumably exists in humans, but that has not yet been determined. Knowing which molecules and cells are involved will help scientists study how humans perceive itch signals.

Before these findings, scientists thought a molecule called gastrin-releasing peptide was responsible for transmitting the itch signal from nerves, and that itching was a low-level form of pain.

Understanding the itch-signaling pathway offers the opportunity to create drugs that specifically block that signal and alleviate unpleasant and chronic itching with fewer side effects.




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