It seems that the age-old wisdom imparted by mothers across the globe holds a scientific truth: Scratching an itch exacerbates the sensation. This intriguing revelation comes from research conducted by a team at the Washington University School of Medicine in St. Louis. Their studies have unearthed that scratching prompts the brain to release serotonin, a neurotransmitter that, paradoxically, heightens the feeling of itchiness.
This groundbreaking research, primarily conducted on mice and published in the prestigious journal Neuron, sheds light on a vicious cycle of itching and scratching that is believed to be similar in humans. It offers fresh insights that could pave the way for novel interventions, particularly for individuals plagued by chronic itching.
For many years, scientists have understood that scratching induces a slight pain that can momentarily divert attention from itching by prompting nerve cells in the spinal cord to transmit pain signals to the brain rather than itch signals. Zhou-Feng Chen, PhD, the study’s senior investigator and director of Washington University’s Center for the Study of Itch, elaborates on the issue. According to Chen, when the brain receives these pain signals, it produces serotonin to mitigate the pain. However, serotonin can inadvertently switch pathways, migrating from pain-sensing neurons to those influencing the intensity of the itch.
Serotonin’s role in pain management has been acknowledged for decades, but its connection to itching has only recently been established through this research. The study involved breeding a strain of mice lacking the ability to produce serotonin. When these genetically engineered mice were exposed to substances that induce itching, they exhibited significantly less scratching than their regular counterparts. Intriguingly, reintroducing serotonin to these modified mice restored their tendency to scratch in response to itch-inducing compounds.
Chen’s insights reveal that although itch and pain signals are transmitted through distinct but interrelated neural pathways, scratching’s temporary relief through minor pain can worsen itching due to the body’s response to pain signals.
Despite the temptation to target serotonin to mitigate itching, Chen cautions against this approach due to serotonin’s vital roles in various bodily functions, including growth, ageing, bone metabolism, and mood regulation. Blocking serotonin outright could have widespread adverse effects, given its importance in natural pain control and its use in treating depression through medications like Prozac, Zoloft, and Paxil.
Instead, the research suggests a more targeted strategy might be feasible, focusing on disrupting the interaction between serotonin and specific nerve cells in the spinal cord responsible for transmitting itch signals, known as GRPR neurons. The team identified the receptor through which serotonin activates these neurons, 5HT1A. By blocking this receptor, they significantly reduced scratching in mice.
Chen’s research unravels the complexities of the itch-pain cycle and reinforces the sage advice to avoid scratching. As the team delves deeper into understanding the molecular and cellular mechanisms underlying this cycle, the simple counsel to resist the urge to scratch gains scientific faith, echoing the wisdom passed down through generations.
More information: Zhou-Feng Chen et al, Descending Control of Itch Transmission by the Serotonergic System via 5-HT1A-Facilitated GRP-GRPR Signaling, Neuron. DOI: 10.1016/j.neuron.2014.10.003
Journal information: Neuron Provided by Washington University School of Medicine
