Following an injury, the normal bodily response is to develop a long-term associated pain response until the body is able to fully recover. A direct result of this response is the reliance on prescribed pain medications, like opioids, to help mitigate pain severity. The dependence on opioids to help manage pain has significantly advanced the current opioid crisis in the United States. A new study from Harvard Medical School investigated neurons and the neuronal pathway involved in the development of long-term pain responses following an injury.
The research team focused on a set of neurons, Tac1 neurons, that are found in the lower portion of the spinal cord and enable communication between the brain and the body. Before this study was conducted, there was little information on the role of Tac1 neurons and their involvement in pain-forming pathways. For their experiments, two types of mice were used, ones with enabled Tac1 neurons and ones with disabled Tac1 neurons, in order to evaluate responses to various types of pain.
From these experiments, the research team found that the mice with disabled Tac1 neurons did not exhibit the normal pain coping behaviors as seen in the mice with Tac1 neurons due to not being able to produce pain sensations. The team next discovered that the Tac1 neurons connect with another long-term pain forming neuron, Trpv1, essentially discovering a pathway for sustained pain transmission. Although Tac1 neurons are involved in long-term pain formation, they are not involved in reflex pain responses; an example would be drawing a hand away when touching something hot.
Image Source: Viaframe
The most common method of studying pain responses is to focus on the brain and the various regions of the brain that are activated following an injury. However, instead of looking inside the brain, these experiments looked at neurons outside of the brain, allowing for the identification of the mechanism for sustained pain development. The combination of Tac1 and Trpv1 neurons interacting with each other in the spinal cord enables the brain to send pain signals to the rest of the body, producing this long-term pain phenomenon.
This study is significant due to the fact that it could translate to future clinical experiments and treatment options that could help lessen the dependence on prescribed opioids (morphine, oxycodone, and hydrocodone). By targeting these neurons with medications, it could be possible to eliminate long-term pain sensations, taking away the need to prescribe addicting and dependence-forming drugs.
Feature Image Source: Michal Jarmoluk
