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New research is examining how our body perceives and transmits itching to the brain.
Light touches play an important role in our daily lives. Between cuddling, picking up fragile objects and performing tasks that require precision, we use this feeling to guide many of our activities. It is also an essential part of the body's defense system, which tells us, among other things, whether we are covered with biting insects such as ticks or mosquitoes – via this so nice sensation of itching.
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"What's important to remember is that this mechanical itch sensation is distinct from other forms of touch and that this pathway is specialized in the spinal cord," said Martyn Goulding, a professor at the University of Toronto. Salk Institute, lead author of the new study.
The team examined how neurons in the spinal cord transmit these itch signals to the brain. They hope that these discoveries will contribute to the development of new drugs to treat chronic itching, such as eczema, diabetes and even certain types of cancer.
Goulding and his colleagues had previously found a set of inhibitory neurons in the spinal cord that kept the itch route blocked most of the time. Inhibitory neurons act as brakes on neuronal circuits, slowing down their activity. Without these neurons, which produce the neurotransmitter neuropeptide Y (NPY), the pathway is constantly active and causes chronic itching.
The team wanted to know how the signal encoding this sensation is transmitted to the brain, which makes us feel itchy. One of the team's assumptions was that when NPY inhibitory neurons are absent, the nerve bundles of the spinal cord that transmit a light touch remain stuck on the "activated" setting, creating an auto-amplifying loop. The team has identified a population of such neurons (excitators) in the spinal cord that express the NPY receptor, the so-called Y1 spinal neurons.
To check if they were actually behind the self-ameliorating itch loop, the team selectively removed the NPY "brake" and Y1 "accelerator" neurons in the mouse to see the effects.
According to them, without the Y1 neurons, the mice did not get scratched, not even in response to mild stimuli that normally make them scratchy. When the team gave them drugs to activate the Y1 neurons, the mice spontaneously gratified themselves, even in the absence of stimuli to the touch. The team was then able to link NPY neurotransmitter levels to the excitability of Y1 neurons – thus showing that NPY controls our sensitivity to light touch. The results are also corroborated by other research that has shown that people with psoriasis have below average levels of NPY.
Although the study shows how itchy signals cross the spinal cord, additional research is needed to understand the entire process. The team explains that other neurons are probably responsible for its transmission and its final response in the brain.
"By developing mechanisms by which mechanical itching is reported under normal circumstances, we will then be able to solve the problem of chronic itching," says David Acton, a postdoctoral researcher at Goulding's lab and lead author of the study.
The document "Neurons expressing the neuropeptide Y1 receptors of the spine is an essential excitatory mechanism for mechanical itching" was published in the journal Cell reports.
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