By discovering a new mechanism through which pain stimuli are relayed to the brain, researchers at the University of Leeds may have just enabled the scientific community to develop improved painkillers for a wide array of conditions.
In addition, the discovery helps explain why current efforts to develop working painkillers have been plagued by failure most of the time. Through the new conclusions, the UK scientists set the foundations for a novel approach to conducting this type of research.
The investigation group was led by UL Faculty of Biological Sciences (FBS) Institute of Membrane and Systems Biology associate professor, Dr. Nikita Gamper. Her team was focused on understanding the difference between persistent pain and pain resulting from increased nerve sensitivity.
An example of the former is toothache. Pain stemming from increased nerve sensitivity is different. It arises, for example, when we touch a wounded or inflamed patch of skin, and is called hyperalgesia.
Details of the new study were published in the May 14 early online issue of the esteemed journal Proceedings of the National Academy of Sciences (PNAS), in a paper entitled “Reactive oxygen species are second messengers of neurokinin signaling in peripheral sensory neurons.”
The main conclusion the new research yielded is that both types of pain are generated by the same nerves, but that the mechanisms underlying these two processes are different, and should be treated as such. The Wellcome Trust and the Medical Research Council funded this investigation.
“Pain originates from a series of electrical signals sent by nerve cells in to the central nervous system and ultimately the brain. Despite much progress, we still don't know enough about the mechanisms by which these pain signals are generated,” Dr. Gamper explains.
“However, this research has shown that whilst the sensation of pain can be similar between various conditions, the underlying molecular mechanisms may in fact be very different,” she goes on to say.
The research draws attention to the fact that current efforts to develop more efficient painkillers do not take into account the exact mechanism through which the pain they are created to address arises. This study therefore suggests that a new approach to researching this class of drugs needs to be taken.
“For instance, drugs for persistent pain are often tested solely for their ability to reduce hyperalgesia, and as a result, some of the drugs that are effective in the lab, fail in subsequent clinical trials,” the University of Leeds team leader concludes.