UNE researchers study on pain sensitivity published in neuroscience journal

Derek Molliver, Ph.D., professor in the Department of Biomedical Sciences and Diana Goode, Ph.D., assistant professor in the Department of Biomedical Sciences, recently conducted research on pain sensitivity that they hope will eventually lead to the development of more effective treatments for pain and perhaps different treatments for men and women.

Their study, “Regulation of mitochondrial function by Epac2 contributes to acute inflammatory hyperalgesia,” is now published in The Journal of Neuroscience, a weekly peer-reviewed scientific journal published by the Society for Neuroscience. It covers empirical research on all aspects of neuroscience.

After an injury, damaged tissue releases inflammatory chemicals that attract cells of the immune system to promote healing. These chemicals also make pain-sensing neurons (known as nociceptors) hyperactive, sending more intense pain signals to the brain, which causes painful hypersensitivity.

Scientists have known for some time that a molecule inside neurons called cAMP acts as a signal to make these pain-sensing neurons more sensitive to touch. What is not clear is how the cAMP makes neurons more sensitive.

Goode and Molliver found that when prostaglandins are applied to nociceptor neurons grown in a dish or injected into the skin in mice, cAMP activates a chain reaction that causes the neurons’ mitochondria to become more active.

Prostaglandins are a group of lipids made at sites of tissue damage or infection that are involved in dealing with injury and illness. They control processes such as inflammation, blood flow, and the formation of blood clots. Mitochondria is important for producing energy for the neuron. The increase in mitochondrial activity may be important for the neurons to be able to continue sending pain signals to the brain, which requires large amounts of energy. By adding a drug that decreases mitochondrial function, Goode and Molliver were able to reduce the hypersensitivity of the pain-sensing neurons caused by the prostaglandins. This study demonstrates a previously unknown way that tissue injury causes pain: by increasing the function of mitochondria in pain-sensing neurons.

Another exciting observation in this study was that the decrease in pain resulting from the mitochondrial suppressant drug was observed in male mice but not in females, even though female mice also get hypersensitive in response to prostaglandins. The scientists deduced that females likely use a different communication pathway to transmit pain in response to injury. One of the important next steps is to figure out what the alternative mechanism is that causes pain in females.

This study is the first publication from a grant awarded to Molliver by the National Institute for Neurological Disorders and Stroke (NINDS) to study neuronal signaling pathways that cause acute and chronic pain.