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They discover why we can not stop scratching when we're bitten


Posted on 12/17/2018 8:00:36CET


It's a crazy bike that has affected us all: it starts a itch that causes scratches, but scratches reinforce itching. Now, researchers have revealed the brain's mechanism that drives this uncontrollable feedback loop that will make us manage. In a study published on Thursday in the Neuron newspaper, researchers showed that the activity of a small subset of neurons, which lies in a deep brain region called periaqueductal gray matter, traces the behavioral behavior induced in mice.

"There is still no effective treatment for chronic itching, which largely depends on our limited knowledge of the neural mechanism of itching," said the study's lead author, Yan-Gang Sun, from the US Academy of Sciences. China. "Our study is the starting point for further deciphering how itching is machined and modulated in the brain, which can eventually lead to the identification of new therapeutic goals," he adds.

Itching can be caused by a wide range of causes including allergic reactions, skin conditions, irritations, parasites, diseases, pregnancies and cancer treatments. The cycle of itchy itching can significantly affect the quality of life and cause serious damage to the skin and tissues.

New studies have identified specific subtypes of neurons in the spinal cord, including cells expressing the gastrin releasing peptide receptor (GRPR). However, relatively little is known about brain regions involved in the treatment of the bran. Sun and his team suspected that periaqueductal gray may be involved, in part because of its critical and well-known role in the treatment of related sensory information, such as pain.


In the new study, researchers first detected periaqueductal mucosa neurons in mice moving freely and induced to scrape by injections with histamine or with a antimalarial drug called chlorokine. The scar behavior induced by itching gave clues to the activity of a specific set of neurons that produce a neurotransmitter called glutamate and a neuropeptide called tachykinin 1 (Tac1).

When the researchers removed the neurons expressing Tac1, the stickiness decreased significantly. In contrast, stimulation of these neurons stimulated a spontaneous scratch behavior, even without histamine or chlorokin, by activating the neurons expressing GRPR in the spinal cord.

Sun says that little is known about how itching the circuit developed, despite its importance to animal survival. "Itchy sensation plays a key role in detecting harmful substances, especially those that have clogged in the skin," said Sun. "Because itching leads to scratches, it allows the animal to get rid of the substances. In some cases, damage caused by scratches can cause strong immune responses, which can help fight the invaded subjects."

In future studies, Sun and his team plan to investigate which molecules of periaqueductal neurons that express Tac1 can be attacked by drugs. They will also look for other nodes in the brain's chirp. "These studies help us to design new approaches or develop new drugs for the treatment of chronic itchy patients," he concludes.

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