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Persistent Pain: Scientists Identify Key Brain Cells for Chronic Pain Sensation

Brain Region Key to Chronic Pain Identified, ​Offering‌ Potential for New Therapies

Researchers have pinpointed a specific area within the brain – the parabrachial nucleus -⁢ that plays a crucial role in the development of chronic pain, potentially opening avenues for novel⁢ treatment strategies. The study, published in Nature on October 8th, reveals a subset​ of neurons within this ⁢region that remain ​active long after an initial injury, contributing to persistent pain.

The ⁢research, conducted on mice,⁤ suggests that this prolonged⁤ neural activity isn’t simply a continuation of the initial pain signal, but a distinct state ⁢linked to the experience‍ of chronic pain, ‌which affects approximately one in five people worldwide. “Pain is in your head. But ‌it​ is indeed very real,” explains Nicholas Betley, a⁣ biologist‌ at the University of Pennsylvania in Philadelphia⁢ and a co-author of the study.

The⁤ team discovered that ⁤these neurons, carrying receptors for a signalling⁣ molecule called neuropeptide Y, switch on following a painful stimulus ⁢like nerve‌ damage ⁣and continue firing even after the initial injury has ‌healed.Artificially activating these ‘Y1R’⁣ neurons ⁢in⁣ mice induced ⁣pain-associated behaviors, while blocking their activity reduced persistent pain ⁣without ⁤impacting ⁢normal, short-lived ⁢pain responses ‌to immediate threats like heat.

“The Y1R neurons alone don’t cause the feeling of pain,” Betley clarifies, “But, they form part of the network ‘that leads to the sensation that we refer to as pain’.”

Interestingly, the study also revealed the brainS own ‍potential⁣ pain-killing mechanism.When mice experiencing chronic pain were subjected to stressors like food or water deprivation, or exposure to a frightening‌ stimulus ⁢(such as bobcat‌ urine), their persistent pain⁤ decreased. ⁣This reduction correlated with ​an influx of neuropeptide Y ‍into the parabrachial nucleus, released by neurons activated by these urgent needs.

Co-author Ann Kennedy,‌ a neuroscientist at the Scripps Research Institute in La Jolla, California, explains‍ this finding: “We think of pain as just a sensory​ input … ‌but the sensation of pain is a lot more malleable, and it’s changed by our experiences.” The researchers hypothesize that when faced with more ​pressing needs, the brain prioritizes those‍ over pain, effectively dampening the activity of the persistent-pain neurons.

If⁤ these findings are confirmed in ⁢humans, they could lead to the development of new therapies targeting the ​parabrachial nucleus and neuropeptide Y signaling to alleviate chronic pain.

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