Parabrachial neurons promote nociplastic pain.

Autor: Palmiter RD; Departments of Biochemistry and Genome Sciences, Investigator of the Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. Electronic address: palmiter@uw.edu.
Jazyk: angličtina
Zdroj: Trends in neurosciences [Trends Neurosci] 2024 Sep; Vol. 47 (9), pp. 722-735. Date of Electronic Publication: 2024 Aug 14.
DOI: 10.1016/j.tins.2024.07.002
Abstrakt: The parabrachial nucleus (PBN) in the dorsal pons responds to bodily threats and transmits alarm signals to the forebrain. Parabrachial neuron activity is enhanced during chronic pain, and inactivation of PBN neurons in mice prevents the establishment of neuropathic, chronic pain symptoms. Chemogenetic or optogenetic activation of all glutamatergic neurons in the PBN, or just the subpopulation that expresses the Calca gene, is sufficient to establish pain phenotypes, including long-lasting tactile allodynia, that scale with the extent of stimulation, thereby promoting nociplastic pain, defined as diffuse pain without tissue inflammation or nerve injury. This review focuses on the role(s) of molecularly defined PBN neurons and the downstream nodes in the brain that contribute to establishing nociplastic pain.
Competing Interests: Declaration of interests The author declares no conflicts of interest.
(Copyright © 2024 The Author. Published by Elsevier Ltd.. All rights reserved.)
Databáze: MEDLINE
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