A way to "turn off" chronic pain has been found

Scientists from the University of Pennsylvania (USA) have discovered a group of neurons whose blockage helps alleviate chronic pain, including headaches. The research results were published on the Nature portal.
During experiments on laboratory mice, scientists identified a special population of nerve cells that were activated after the initial pain stimulus - for example, when a nerve was damaged. This group of neurons remained active even after the stimulus ended.
The cells were distributed throughout the parabrachial nucleus of the brain.
This area is involved in the transmission of pain signals, as well as in the regulation of breathing, sleep, fear response, and other basic physiological processes.
Scientists discovered that the neurons contained receptors for the signaling molecule neuropeptide Y (Y1R receptors). When researchers artificially activated neurons with such receptors, mice exhibited behavior characteristic of pain sensations. When these neurons were blocked, manifestations of chronic pain weakened, however, the acute pain response to dangerous stimuli (such as touching a hot surface) was preserved.
"Y1R neurons themselves do not cause pain, but they participate in the formation of a persistent pain signal. They can be considered part of a broader neural network associated with the perception of chronic pain," noted the study leader, Professor Jeremy Betley.
In a separate series of experiments, mice with signs of persistent pain were subjected to various stressful influences - for example, they were deprived of food and water or placed in an environment with the smell of predator urine. These conditions led to a decrease in pain response: animals experiencing hunger did not react to touching damaged limbs two weeks after the injury. This allowed scientists to suggest the presence of an innate pain suppression mechanism in mice that is activated during prolonged starvation.
According to the researchers, the discovery may be useful for further study of the molecular mechanisms of chronic pain. In the future, blocking Y1R neurons may prove effective for humans as well, but additional experiments are needed to confirm this hypothesis.
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