This weekend I suffered what many people do on a regular basis – low back pain that affected just about every direction in which I turned. I tried stretching, complaining, heat, complaining some more before finally surrendering to ibuprofen and landing on my couch.
So, it was with special interest when I read that scientists have identified a gene responsible for chronic pain, with hopes it could lead to the development of drugs for treating chronic back pain. This is exciting news for those with chronic pain.
Researchers at the University of Cambridge in the United Kingdom removed the HCN2 gene from pain-sensitive nerves in mice (Science 9 September 2011: 1462-1466). They found that deleting the gene stopped any chronic pain but did not affect acute pain (the type you feel when you’ve slammed your finger in the car door).
Chronic pain comes in two forms: inflammation stemming from a burn or arthritis or neuropathic pain, in which nerve damage causes ongoing pain and a hypersensitivity to stimuli. Neuropathic pain is seen in patients with diabetes and shingles, following chemotherapy and in lower back pain. Neuropathic pain — often lifelong — is very difficult to treat with current drugs.
The goal now is to develop new drugs that could block the protein produced by the HCN2 gene to combat chronic back pain.
The HCN2 gene, which is expressed in pain-sensitive nerve endings, has been known for several years, but its role in regulating pain was not understood.
The researchers studied genetically modified mice in which the HCN2 gene had been deleted. By measuring the speed the mice withdrew from different types of painful stimuli, the scientists were able to determine that deleting the HCN2 gene abolished neuropathic pain. Interestingly, they found that deleting HCN2 does not affect normal acute pain. This is important because normal pain sensation is essential for avoiding accidents.
“Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation,” says Professor Peter McNaughton, lead author of the study and head of the department of pharmacology at the University of Cambridge. “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.”
The study was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), and the European Union.