The itch that comes along with a mosquito bite can be quite irritating, but the sensation can be remedied by existing treatments.
Chronic itch, on the other hand, is highly unpleasant and a lot harder to treat. It can cause significant skin and tissue damage and impair one’s quality of life.
According to a study published last year, chronic itch affects about 10% of the population. Many people are treated with immune suppressants which often fail to provide relief and may end up causing severe side effects.
Now, new research has found that, unlike other touch sensations, the itch sensation has a specialised route within the spinal cord. These findings may contribute to a better understanding of itch and help to develop new drugs to treat chronic itch, which commonly occurs in conditions such as diabetes, eczema and some cancers.
The study, published in the journal Cell Reports, was led by Salk Institute researchers. The researchers discovered how a set of neurons in the spinal cord help transmit light-touch signals from the skin to the brain.
Chronic itch accelerator stuck in 'on' position
Salk professor Martyn Goulding, senior author of the study, and his colleagues had previously discovered a set of inhibitory neurons that act as cellular brakes. Their job is to keep the mechanical itch pathway in the spinal cord turned off most of the time. These neurons produce the neurotransmitter Y (NPY); without it, the pathway is left constantly on.
Under normal circumstances, the itch signal is suppressed by the NPY neurons. However, the researchers didn’t know how the itch signal is transmitted to the brain to register the itch sensation.
Researcher David Acton hypothesized that when the NPY inhibitory neurons are missing, neurons in the spinal cord that typically transmit light touch begin to act like an accelerator stuck in the ‘on’ position, causing chronic itch.
'NPY neurons act as a thermostat'
To test whether these neurons truly were acting like an accelerator, Acton performed another experiment that involved selectively getting rid of both NPY (‘brake’) and Y1 (‘accelerator’) neurons. (The so-called Y1 spinal neurons transmit the itch signal in the spinal cord, and is therefore labelled the ‘accelerator’ neurons.)
It was found that without the Y1 neurons, mice didn’t scratch, even in response to light-touch stimuli that would normally make them do so. When Acton gave them drugs that activated the Y1 neurons, they scratched spontaneously, even in the absence of touch stimuli.
This means that the NPY neurotransmitter acts as a kind of thermostat to control our sensitivity to light touch. People with psoriasis, for example, have lower than average levels of NPY and their 'brakes' on the Y1 neurons are less effective, leading them to itch more than people without the condition.
Although the researchers have dug deep into finding the mystery neurons thought to be responsible for mediating the final response in the brain, they encourage further research on the topic to continue mapping out the full pathway. This will ultimately help suggest targets for drugs to reduce the itching sensation in people who are overly responsive, and could potentially lead to solutions to treat chronic itch.