Researchers at Karolinska Institutet in Sweden suggest that after nerve damage has occurred, a neuron that usually allows the sensation of pleasant touch can switch function and instead signal pain.
In their study, published recently in Science, they suggest that a small RNA molecule (microRNA) in sensory neurons regulates how touch is perceived. Upon nerve damage, levels of this molecule drop in the sensory neurons, which results in raised levels of a specific ion channel that makes the nerve cells sensitive to pain.
“Our study shows that touch-sensitive nerves switch function and start producing pain, which can explain how hypersensitivity arises,” says Professor Patrik Ernfors at Karolinska Institutet’s Department of Medical Biochemistry and Biophysics, in a media release from Karolinska Institutet. “MicroRNA regulation could also explain why people have such different pain thresholds.”
“Nerve pain is a complex condition with several underlying mechanisms,” Ernfors adds. “What’s interesting about our study is that we can show that the RNA molecule controls the regulation of 80 percent of the genes that are known to be involved in nerve pain. My hope, therefore, is that microRNA-based drugs will one day be a possibility.”
The research was primarily conducted on mice but also verified in tests on human tissue, where low microRNA levels could be linked to high levels of the specific ion channel and vice versa, suggesting that the mechanism is the same in humans.
“It’s vital that we understand the mechanisms that lead to chronic nerve pain so that we can discover new methods of treatment,” Ernfors continues. “The pharmaceutical companies have concentrated heavily on substances that target ion channels and receptors in pain neurons, but our results show that they might have been focusing on the wrong type of neuron.”
[Source(s): Karolinska Institutet, Science Daily]
