Scientists Discover a Protein That Helps Control Pain, Touch and Itch

Scientists have identified a previously underappreciated protein that plays an important role in how the nervous system responds to pain, temperature, touch and itching. The discovery could eventually help researchers develop more targeted treatments for chronic pain and other sensory disorders.

The research, published in Nature Neuroscience and reported on November 2, 2026, reveals that a protein called CRELD1 helps nerve cells transmit electrical signals after detecting physical stimulation. In experiments involving mice, removing this protein significantly reduced their sensitivity to several different sensations, including heat, cold, pressure and itch.

The findings suggest that sensations we normally consider separate may depend on a shared molecular mechanism inside the nervous system.

How the Human Body Detects Pain and Temperature

Every day, our bodies process an enormous amount of sensory information. When we touch a cold surface, feel pressure against our skin or experience sudden pain, specialized nerve endings detect changes in the environment and communicate with the brain.

This process happens extremely quickly. Sensory receptors respond to physical or chemical stimulation, while nerve cells generate electrical impulses that travel through the nervous system. The brain then interprets these signals, allowing us to recognize what we are feeling.

Different sensory experiences depend on specialized biological mechanisms. Some receptors respond to temperature, while others detect pressure, tissue damage or substances associated with itching.

However, researchers have now discovered that several of these pathways share an important molecular component responsible for strengthening the signals produced by sensory neurons.

The Discovery of CRELD1

A research team led by scientists at Tsinghua University in China investigated genes that influence how animals respond to sensory stimulation.

Using CRISPR gene-editing technology, the researchers disabled selected genes in mice and examined how the animals reacted to touch, temperature and other physical sensations. Among the genes investigated, one called Creld1 produced particularly interesting results.

Mice lacking the protein showed weaker responses to gentle touch and painful pressure. They were also slower to react to hot and cold surfaces, suggesting that CRELD1 contributes to several different sensory pathways.

The animals also displayed significantly reduced scratching behavior when exposed to substances that normally trigger itching.

These changes were not explained by a general inability to move. The researchers reported that the animals maintained normal body weight, movement and coordination during the experiments.

This suggested that CRELD1 was specifically influencing the processing of sensory information.

A Hidden Mechanism Inside Nerve Cells

To understand how the protein works, scientists examined the electrical activity of sensory neurons.

They discovered that the nerve cells could still detect stimulation even without CRELD1. The difficulty appeared during the next stage, when the cells attempted to generate electrical impulses.

Neurons use specialized proteins called sodium channels to produce the electrical signals that travel through the nervous system. These channels allow electrically charged sodium ions to move across cell membranes, helping initiate nerve impulses.

The researchers found that CRELD1 interacts with several sodium channels and strengthens their activity. Without the protein, neurons required stronger stimulation to generate electrical signals and produced fewer impulses.

When scientists increased CRELD1 production, the opposite effect occurred. The nerve cells generated stronger electrical responses, and the animals became more sensitive to certain sensations.

The results suggest that CRELD1 acts as a regulator of sensory signaling rather than as a receptor that directly detects pain or temperature.

Could This Discovery Lead to Better Pain Treatments?

Chronic pain affects millions of people worldwide and can significantly interfere with everyday activities. Although many medications are available, some provide limited relief or produce unwanted side effects.

The newly identified mechanism may offer researchers another possible target for developing treatments that modify how pain signals travel through the nervous system.

By influencing the interaction between CRELD1 and sodium channels, future medicines might potentially reduce excessive sensory signaling without completely blocking nerve function.

However, such applications remain theoretical. The latest experiments were primarily conducted in mice, and the researchers have not demonstrated that manipulating CRELD1 can safely treat pain in humans.

Scientists also face an important challenge: pain, temperature and touch are essential protective sensations. A treatment that reduces harmful pain must ideally preserve the body's ability to recognize dangerous situations.

For example, the ability to feel extreme heat allows a person to withdraw their hand from a hot surface before serious injury occurs.

Any future medication based on this discovery would therefore require careful testing to avoid interfering with normal protective responses.

Researchers Still Need to Understand the Human Protein

Although CRELD1 is also present in humans, its behavior may not be identical to what researchers observed in mice.

The scientists examined two human versions of the protein in laboratory-grown cells and found that they did not affect sodium-channel activity in exactly the same way.

One version strengthened the activity of a tested sodium channel, while the other did not produce the same effect.

This difference suggests that researchers must investigate which versions of CRELD1 are present in human sensory neurons and how they function under normal biological conditions.

Additional studies will also be necessary to determine whether the protein influences different kinds of pain equally or whether its effects vary between tissues and sensory pathways.

What the Discovery Means for Neuroscience

The findings provide new insight into how the nervous system transforms physical stimulation into electrical information.

For decades, scientists have investigated the receptors that allow humans and animals to detect pain, temperature and pressure. This research adds another layer to that understanding by identifying a protein that helps determine how strongly nerve cells communicate after stimulation occurs.

The discovery may also encourage further research into conditions involving unusual sensitivity to touch, persistent itching or chronic pain.

While the findings do not represent an immediate medical breakthrough or an available treatment, they reveal an important piece of the complex biological machinery responsible for our everyday sensations.

Every touch, sudden change in temperature and uncomfortable itch depends on an intricate network of cells and molecular processes. By identifying another component of that network, scientists are moving closer to understanding how the body experiences the physical world.

The research demonstrates that even the most familiar human sensations still contain biological mysteries waiting to be explored.

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