They find out why we can not stop scratching when we're bitten


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

MADRID, December 17 (EUROPE PRESS) –

It is a maddening cycle that has affected us all: it starts an itch that causes scratches, but scratching only worsens the itching. Researchers have now revealed the mechanism of the brain that drives this cycle of uncontrollable feedback that makes us scratch. In a study published Thursday in the journal "Neuron," scientists have shown that the activity of a small subset of neurons, located in a deep region of the brain called periaquedutal gray matter, traces the scratching behavior evoked in mice.

"There is still no effective treatment for chronic itching, which is largely due to our limited knowledge about the neural mechanism of itching," says lead author of the study, Yan-Gang Sun, of the US Academy of Sciences. "Our study provides the starting point for further deciphering how the itch is processed and modulated in the brain, which could lead to the identification of new therapeutic targets," he adds.

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

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

The role of neurons that produce a neurotransmitter

In the new study, scientists first recorded the periaqueductal gray matter neurons in freely moving mice that were induced to scratch through histamine injections or an antimalarial drug called chloroquine. The itching-induced scratching behavior 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 Tac1-expressing neurons, the itching-induced scratching decreased significantly. In contrast, stimulation of these neurons triggered spontaneous scraping behavior, even without histamine or chloroquine, activating neurons expressing GRPR in the spinal itch circuit.

Sun says little is known about how the itch circuit has evolved, despite its importance to the survival of animals. "The itching sensation plays a key role in the detection of harmful substances, especially those that adhere to the skin," says Sun. "Since itching leads to the risk of itching, it allows the animal to get rid of the substances. In some cases , the scratching injury can cause strong immune responses, which could help fight the invaded substances. "

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


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