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Could Hunger Alter Responses to Chronic Pain?

April 12, 2018
Researchers at the University of Pennsylvania pinpoint new targets for treating pain

To ensure one’s survival, the brain’s process of hunger and pain are both competing signals that must resolve each other in order to properly function. The neural pathways of conflicting survival responses and needs, however, are still being put into question and are not fully understood in the medical literature. According to research from Alhadeff et al,1 hunger may weaken the behavioral responses and properties of inflammatory pain without altering acute nociceptive pain responses in mice.

By observing mice that had not eaten for a day, the research team looked at responses to acute pain as well as long-term inflammatory pain, and their corresponding neural circuits in the brain. While acute responses remained the same, hungry mice were less responsive to the inflammatory pain, a response similar to taking a painkiller. The hungry mice with inflammatory pain also did not avoid a place where they had been exposed to the pain, as opposed to fed mice.1

The researchers looked at this intersection in the brain between hunger and chronic pain responses, starting with the centrally controlled activity in hunger-sensitive agouti-related protein (AgRP)-expressing neurons, which was shown to diminish inflammatory pain. According to the paper, further analysis revealed that the neural processing of hunger and inflammatory pain converged in the hindbrain parabrachial nucleus (PBN). Diving deeper, the anti-nociceptive effect of hunger was found to be mediated by neuro-peptide Y (NPY) signaling in the PBN, which became a target for pain suppression. Blocking the receptors for NPY reversed the effects of hunger, and the chronic pain returned in the mice.1

This work in pinpointing the brain cells responsible for prioritizing hunger over chronic pain (with acute pain responses staying the same) offers new opportunities for potential therapies in the treatment of chronic pain. If these findings become relevant in further studies in humans, these results may offer a future target for chronic pain after injuries, as a way to complement or outright replace the opioid medications that are usually prescribed for symptoms.

“This unexpected ability to influence pain through activity in a distinct hypothalamic-hindbrain hunger circuit reveals an endogenous and ethologically relevant neural circuit mechanism for analgesia,” the study authors concluded.

Last updated on: April 19, 2018
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Psychological Flexibility May Lead to Better Response to Pain Treatments
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