It is the neurons in the spinal cord that transmit the signals to the brain that trigger the itch. Researchers have just found out how it happens.
Does it tickle you, does it tickle you? It’s your sense of light touch that has just picked up a signal telling your brain to protect you against a threat aimed at your skin. This light touch plays an essential role in tasks of daily life: delicately grasping a fragile object, playing a stringed instrument, for example.
But this sensation, the itch, is above all an important part of our defense system by alerting us to what, in our environment, could make us fall, injure or attack us such as biting insects such as those that cause malaria or Lyme disease.
Itching can become chronic
But how are these signals triggered? Researchers have just discovered how neurons in the spinal cord help transmit them to the brain. Their findings which have just been published in the journal Cell Reports provide a better understanding of the mechanism of itching. And the prospects of the result of this work are important since they go as far as the possibility of finding new drugs against the itch which, beyond the small daily ailments, can become chronic in diseases such as eczema, diabetes or certain cancers.
“The takeaway is that this mechanical itch sensation is distinct from other forms of touch and that this pathway is located in the spine,” says Professor Salk Martyn Gouldind, lead author of the study.
He and his colleagues had previously discovered a set of inhibitory neurons in the spinal cord that keep the mechanical itch pathway in it disabled. Without these neurons that produce a neurotransmitter, neuropeptide Y (NPY), the mechanical itch pathway is permanently activated, causing chronic itch. But the researchers didn’t know how the itch signal, normally suppressed by NPY neurons, is transmitted to the brain to cause the itch sensation.
A throttle stuck in the “on” position
They then hypothesized that when NPY inhibitory neurons are missing, neurons in the spinal cord that normally transmit light touch begin to act as an accelerator that would be stuck in the “on” position and they identified a population spinal cord excitatory neurons that express the NPY receptor, Y1 spinal neurons. And they undertook an experiment in mice to selectively dump the “brake” and “accelerator” neurons of the NPY. They thus demonstrated that NPY signaling acted as a sort of thermostat based on the excitability of Y1 neurons and allowing us to control our sensitivity to touch.
Lower than average NPY levels in patients with psoriasis
Data from other laboratories also show that patients with psoriasis had lower than average levels of NPY.
While Y1 neurons transmit the signal to itch in the spinal cord, other neurons may be responsible for mediating the final response in the brain, but further research, according to Salk Martyn Goulding’s team, would be needed to map the full pathway and suggest drug targets to lessen the itch sensation in overly reactive people and find ways to combat chronic itch.
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