A gene called HCN2 produces a protein which regulates chronic pain, researchers from Cambridge University, England, and the University of Cadiz, Spain reported in the journal Science. They added that medications which inhibit the gene’s protein production could be extremely effective in combating chronic pain.

Chronic pain, also known as persistent pain, is long-term pain that lasts over 12 weeks, or pain that continues after healing is completed and pain should have stopped, as may be the case after surgery or trauma.

Chronic pain is estimated to affect about 1 in every 7 people in the UK. In the USA, the NIH (National Institutes of Health) says that up to 56 million adults suffer from chronic pain, that’s 28% of all adults in the country – 4 million have neuropathic pain, 20 million have jaw and lower facial pain, 25 million have migraine pain, 48 million have arthritis pain, and 16 million have lower-back pain.

There are two main types of chronic pain:

  • Inflammatory pain – this occurs when a persistent injury causes the nerve endings to become much more sensitive, consequently raising the sensation of pain.
  • Neuropathic pain – nerve damage causes continuous pain. Current drugs are not very good at treating this common condition. Patients with diabetes, shingles, those undergoing or who underwent chemotherapy, lower back pain, and some other conditions have a significantly higher risk of being affected by this kind of pain.

Lead author, Prof. Peter McNaughton, head of the Dept. of Pharmacology at the University of Cambridge, said:

“Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications. Our research lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2.”

Experts have known about the HCN2 gene, which is present in pain-sensitive nerve endings, for a long time. However, nobody fully understood what its role was in regulating pain.

Scientists had mistakenly assumed that HCN2 might have been regulating electrical frequency activity in pain-sensitive nerve endings, because HCN4, a related gene, is closely involved in controlling electrical frequency activity in the heart.

In this study, the scientists removed the HCN2 gene from the pain-sensitive nerves. They then used electrical stimuli on these nerves in cell cultures to find out how their properties might change after the HCN2 gene had been removed.

The in-vitro studies in cell cultures provided promising results. So, the researchers moved onto studying genetically modified mice which had had the HCN2 gene deleted. They were able to determine that the elimination of the HCN2 gene got rid of neuropathic pain by measuring how quickly the mice moved away from various types of painful stimuli.

They were surprised to find that the deletion of the HCN2 gene did not affect their response to acute pain. Examples of acute pain are, biting your tongue, or touching something extremely hot. Acute pain comes on rapidly, is usually severe, but goes away fairly quickly.

Professor McNaughton said:

“Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation. What is exciting about the work on the HCN2 gene is that removing it – or blocking it pharmacologically- eliminates neuropathic pain without affecting normal acute pain. This finding could be very valuable clinically because normal pain sensation is essential for avoiding accidental damage.”

Written by Christian Nordqvist