A parabrachial hub for need-state control of enduring pain.
Goldstein N, Maes A, Allen HN, Nelson TS, Kruger KA, Kindel M, Yeung ATM,
Smith NK, Carty JRE, Boccia L, Blank N, Lo E, Villari RE, Cho E, Marble
EL, Awh M, Dumiaty Y, Chee MJ, Khanna R, Thaiss CA, Taylor BK, Kennedy A,
Betley JN.
Nature. 2025 Nov;647(8090):689-697. doi: 10.1038/s41586-025-09602-x.
Epub 2025 Oct 8.
PMID: 41062698

Abstract
Long-term sustained pain following acute physical injury is a prominent
feature of chronic pain conditions1. Populations of neurons that rapidly
respond to noxious stimuli or tissue damage have been identified in the
spinal cord and several nuclei in the brain2-4. Understanding the
central mechanisms that signal ongoing sustained pain, including after
tissue healing, remains a challenge5. Here we use spatial
transcriptomics, neural manipulations, activity recordings and
computational modelling to demonstrate that activity in an ensemble of
anatomically and molecularly diverse parabrachial neurons that express
the neuropeptide Y (NPY) receptor Y1 (Y1R neurons) is increased
following injury and predicts functional coping behaviour. Hunger,
thirst or predator cues suppressed sustained pain, regardless of the
injury type, by inhibiting parabrachial Y1R neurons via the release of
NPY. Together, our results demonstrate an endogenous analgesic hub at
pain-responsive parabrachial Y1R neurons.

https://www.nature.com/articles/s41586-025-09602-x
(先頭にhを付けてください)