Experiencing an itch is for most people a simple, transient irritation – and often a useful thing, signaling the presence of a previously unknown abrasion, or insect bite or stubborn bit of twig lodged in the fabric of a jumper.
In some cases, however, the itch never goes away, and causes significant problems. A 2016 Spanish study found that “chronic itching has significant psychosocial repercussions”, including anxiety and depression.
Clinical remedies for chronic itching are challenging because, despite extensive study, the precise pathway by which itch information is transmitted to the brain, and how that information then stimulates scratching behaviour, have remained mysterious.
Now a team led by Yangang Sun of the Chinese Academy of Sciences, in Shanghai, has traced the itch information neural pathway, at least in mice, raising the prospect of an eventual therapeutic solution.
The scientists investigated exactly how itch-specific neurons located in the spinal cord communicated with the brain. By using several different approaches, including the use of light pulses and synapse-blocking chemicals to influence cell behavior, the team discovered that the signal pathway was less direct than previously assumed.
When stimulated, spinal itch neurons produce gastrin-releasing peptide receptor (GRPR). Using a purpose-bred transgenic mouse line, Sun and his colleagues discovered these receptors do not directly signal the brain. Instead, the signal travels to an area of the brain stem known as the parabrachial nucleus (PBN), travelling a route called the spino-parabrachial pathway.
The PBN was also shown to play a key role in “itch-processing”, the neural action that prompts a scratching response. Sun’s team was able to demonstrate that suppressing activity in the area led to reduced scratching behaviour.
In a paper published in the journal Science, the scientists say the discovery of the primary neural circuit that governs itch processing and scratching should lead to more detailed investigation of the pathways involved.