New neuroscience research analyzing competing behaviors has shown that inflammatory pain is suppressed by the feeling of hunger. The study focused on a small group of 300 brain cells, known to be hunger-sensitive neurons, which have the ability to select hunger over chronic pain. These cells could potentially provide targets for developing new treatments for pain. The study findings were published in Cell.
J. Nicholas Betley’s lab, the team behind the new research, normally studies hunger and how that single need impacts behavior. In this study, they were interested in studying animal behavior when experiencing two competing needs simultaneously.
"We didn't set out having this expectation that hunger would influence pain sensation so significantly," says Alhadeff, lead author of the paper, "but when we saw these behaviors unfold before us, it made sense. If you're an animal, it doesn't matter if you have an injury, you need to be able to overcome that in order to go find the nutrients you need to survive."
The researchers found that compared to the control group, mice that hadn’t eaten for 24 hours still responded to acute pain but were not as affected by inflammatory pain. They responded similarly to mice that had taken anti-inflammatory medication. The results of an additional conditioning experiment demonstrated that the hungry mice did not go near a place where they had been experienced inflammatory pain but the well-fed mice avoided the same area.
Additional research showed that a group of hunger-related neurons, agouti-related protein (AgRP) neurons, made up the brain area responsible for both hunger and pain processing. Experiments activating these neurons demonstrated that chronic pain responses were reduced as acute pain responses were sustained. With deeper analysis, the team determined that a specific subpopulation of only 300 AgRP neurons that interact with the parabrachial nucleus (PBL) were responsible for significant suppression of inflammatory pain. In addition, neuropeptide Y (NPY), a neurotransmitter, was shown to inhibit inflammatory pain responses. By blocking NPY receptors, hunger was reduced and pain feelings returned.
If the findings are similar in humans, the NPY signaling pathway in the PBL could offer targets for new therapeutics to treat chronic or inflammatory pain.
"We don't want to shut off pain altogether," Alhadeff says, "there are adaptive reasons for pain, but it would be great to be able to target just the inflammatory pain."