Chronic Pain Inhibited By Hunger

Pain can be useful for instance without it as warning one might let a finger linger on or too close to a hot burner on the stove. Chronic inflammatory pain which can linger for longer that can occur after injury can prove to be not only debilitating but also very costly, preventing work and completing important tasks, in  natural settings lethargy triggered by such debilitating pain could prove to even hinder survival.

According to researchers from University of Pennsylvania mice brains have a way to suppress chronic pain that allows the animal to look for food while leaving the response to acute pain intact. A population of 300 brain cells has been found by the team which are responsible for the ability to prioritize hunger over chronic pain. It is hopeful that this group of neurons may offer targets for future developments of novel pain therapies.

The team focused on investigating hunger and how hunger may alter perception. Researchers observed mice which hadn’t eaten for 24 hours and how they responded to either acute pain or long term inflammatory pain. It was found that mice still responded to sources of acute pain but were less responsive to inflammatory pain, behavior was similar to that of mice give painkillers. Researchers found that hungry mice did not avoid a place where they had been exposed to inflammatory pain while mice that weren’t hungry avoided that area in conditioning experiments.

To find out which part of the brain was processing the intersection between pain and hunger researchers experimentally turned on neuron group agouti-related protein AgRP neurons which is activated by hunger and found that acute pain responses stayed intact while chronic pain responses subsided. Next subpopulation AgRP neurons appeared to integrate hunger signals with inflammatory pain, activation of each AgRP subpopulation one at a time it was found that stimulation of only a few hundred project to the parabrachial nucleus suppressing inflammatory pain significantly. Further investigations showed that neurotransmitter molecule NPY is responsible for selectively blocking inflammatory pain responses, blocking NPY receptors reversed effects of hunger and pain returned.

This neural circuit may offer great targets for ameliorating chronic pain which lingers on after injuries and avoid opioid medications which can have adverse side effects and can also inhibit acute pain if results can hold up in humans. With plans to continue on with their efforts to consider how survival behaviors integrate with the brain and how they are processed and prioritized the team will carry on with the next step in the process which is to map out in greater detail and depth how the brain processes inflammatory pain to possibly identify even more targets which may be used to suppress pain.