A new study recently published in the Journal of the Mechanical Behavior of Biomedical Materials have unlocked the secrets behind the makings of the urge to scratch an itch.
The team of researchers has discovered a set of inhibitory neurons that serve as cellular brakes. This said neurons are found in the spinal cord with the task of keeping the mechanical itch pathway “turned off” for the majority of the time.
The research has revealed that neurons in the spinal cord help to transmit signals to the brain which causes the human body to feel an itch and scratch.
The team said that the research could help in contributing a better understanding of what makes one’s skin itch. It can also lead to the invention of new medical drugs that can treat chronic itch.
Conditions such as diabetes, eczema, and some cancers are those that exhibit symptoms such as chronic itch where a person experiences an irritating and uncomfortable sensation to the skin.
Martyn Goulding, a professor at the Salk Institute in California, pointed out that the takeaway for their research is that mechanical itch sensation has a distinction from other forms of touch. The professor also pointed out that mechanical itch sensation has a specialized pathway within the spinal cord.
For those with chronic itch, the team has observed the lack of inhibitory neurons in the spinal cord that produce the neurotransmitter neuropeptide Y (NPY). This would leave the mechanical itch pathway to be constantly “switched on”, leading to uncomfortable chronic itch.
For their research, the team eliminated both the NPY “brake” and the Y1 “accelerator” neurons in the spinal cord of mice. This was done for the team to test whether the said neurons indeed play a role as an accelerator.
As a result of eliminating Y1 neurons, the subject mice did not scratch even if they were subjected to light-touch stimuli, which would have normally made the subject mice scratch.
The mice were later subjected to drugs that activated the Y1 neurons. With this, the mice were observed to scratch spontaneously even without being subjected to light-touch stimuli.
The team pointed out that their research was able to demonstrate how NPY neurotransmitter controls the level of excitability for the Y1 neuron. The team later explained that the NPY signaling plays the role of a “thermostat” that controls the human body‘s sensitivity to light touch.
