Science 3 min read

Scientists Discover How Itch Signals are Transmitted to the Brain

Scientists have identified the neurons that send itch signals to the brain, a discovery that could improve treatment for chronic itch conditions.

Image courtesy of Shutterstuck

Image courtesy of Shutterstuck

Researchers at Salk Institute for Biological Studies have discovered how the neurons in the spinal cord transmit itch signals to the brain.

Light touch is an essential part of our everyday task. Whether we’re picking up a glass of water or a musical instrument, the sensation alerts us to the potential danger of the objects around us.

Also, light touch plays a vital role as one of the defense systems that has evolved to protect us from insect bites. It sends an itch signal to the brain when the insect lands on our skin, raising the urge to scratch.

Now, scientists at Salk have discovered how neurons in the spinal cord transmit these signals to the brain.

In their published paper in the journal Cell Reports, the researchers described how their findings could contribute to a better understanding of itch. With this knowledge, we could one day develop drugs to treat chronic itch in conditions such as diabetes, eczema, and some cancers.

Senior author of the study and Frederick W. and Joanna J. Mitchell Chair, Professor Martyn Gouldingsaid:

“The takeaway is that this mechanical itch sensation is distinct from other forms of touch and it has this specialized pathway within the spinal cord.”

How the Spinal Cord Transmit Itch Signals

In a previous study, the Salk researchers had noticed a set of inhibitory neurons in the spinal cord that acts like cellular “brakes.” Thanks to these neurons, the mechanical itch pathway in the spinal cord remains switched off most of the time.

Conversely, the absence of these inhibitory neurons, which produces neuropeptide Y (NPY), leaves the mechanical pathway open. As you may have guessed, this is the primary cause of chronic itch.

At the time, Goulding and team didn’t understand how the itch signals, which the NPY neurons suppress under normal circumstance, is transmitted to the brain to register the itch sensation. So, they decided to investigate.

A postdoctoral fellow in Goulding’s lab, David Acton had a hypothesis. Acton believed that when the NPY inhibitory neurons are absent, neurons that transmit light touch in the spinal cord suddenly begin to act like an accelerator that’s always in the “on” position.

He then proceeded to identify a candidate for these light touch neurons. It was the Y1 spinal neurons, a population of excitatory neurons in the spinal cord that expresses the receptor for NPY.

Now, Acton had to test if indeed these neurons act like an accelerator.

To do this, the researcher experimented to selectively remove both the NPY “brake” and the Y1 “accelerator” neurons in mice subjects.

With the Y1 neurons absent, the mice didn’t get scratchy even in response to light touch stimuli. However, when Acton administered a drug to activate the Y1 neurons, the mice scratched repeatedly, even without any touch stimuli.

Goulding and colleagues were then able to prove that the NPY neurotransmitter controls how excitable the Y1 neuron would be.

Further research revealed that patients with psoriasis have a lower than average NPY level. In other words, their brake on mechanical itching is not nearly as effective as other people’s.

“By working out mechanisms by which mechanical itch is signaled under normal circumstances, we might then be able to address what happens in chronic itch,” Acton concluded.

Read More: Researchers Derived Sensory Interneurons From Stem Cells for the First Time

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Sumbo Bello

Sumbo Bello is a creative writer who enjoys creating data-driven content for news sites. In his spare time, he plays basketball and listens to Coldplay.

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