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They find out why we can not stop scratching when we bite

Published 12/17/2018 8:00:36CET

MADRID, December 17 (EUROPA-PRESS) –

It's a confusing cycle that has affected us all: itching begins to cause scratching, but scratching only exacerbates the itching. Now scientists have revealed the brain mechanism that drives this uncontrollable feedback loop that gets us scratched. In a study published on Thursday in "Neuron," researchers showed that a small portion of neuronal activity located deep in the brain area called periaqueductal gray traces the scratch behavior in mice.

"Chronic itching has not yet been effective treatments, largely due to the fact that we have little information about itching on the coming neuronal mechanism," says the study's lead author Yan-Gang Sun of the US Academy. China. "Our research provides a starting point to further investigate how itching is treated and modulated in the brain, which can lead to the identification of new therapeutic targets," he adds.

Itching can be caused by a variety of causes such as allergic reactions, skin symptoms, irritants, parasites, diseases, pregnancies and cancer treatments. Scarring by itching can significantly affect the quality of life and cause serious damage to the skin and tissues.

Recent studies have found specific subtypes of neuronal cells in the spinal cord trachea, including cells expressing the gastrin-releasing peptide receptor (GRPR). But relatively little is known about the areas of the brain involved in weaving. The sun and his team suspected that periaqueductal gray might be involved in part because it is a critical and well-known role in dealing with related sensory information, such as pain.

Neuron's role in producing NEUROTRANSMITTER

In the new study, scientists first register the peruvianadductive gray-blooded neurons in mice moving freely and inducing scratches injected with histamine or an anticancer medication called chloroquine. The scarring scarring behavior gave clues to a particular neurons producing a neurotransmitter called Tacylin 1 (Tacl) called glutamate and neurocype.

When researchers removed Tac1 expressed neurons, scarring caused by itching was significantly reduced. In contrast, stimulation of these neurons triggered spontaneous scratching behavior, even without histamine or chloroquine, by activating neurons that express the itching of the GRPR spine.

The sun tells a little about how itching develops, despite its significance in animal survival. "The itching sensation plays a key role in detecting harmful substances, especially skin adhesion," says Sun. "Because itching leads to scratching, it allows the animal to get rid of the substances. In some cases, scarring injuries can cause powerful immune responses that can help fight off attacks."

In future studies, Sun and his team intend to find out which molecules of periaqueductal neurons that express Tac1 can invade drugs. They are also looking for other nodes in the brain itching online. "These studies will help us to design new approaches or develop new medicines for people with chronic itching," he says.

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