Inflammation-induced mitochondrial and metabolic disturbances in sensory neurons control the switch from acute to chronic pain

• DOI: 10.1016/j.xcrm.2023.101265
• Publication Date: 2023-11-08T15:30:41Z
• Authors: Hanneke L.D.M. Wi...; Patrícia Silva Sa...; Melissa Broeks; Nils Meijer; Sabine Versteeg; Annefien Tiggeler; Teun P. de Boer; Jędrzej M. Małecki; Pål Ø. Falnes; Judith Jans; Niels Eijkelkamp
• Keywords: Inflammation; Sensory Receptor Cells; General Biochemistry,Genetics and Molecular Biology; Article; Mitochondria; mitochondria; Mice; sensory neurons; inflammation; Hyperalgesia; redox; Humans; Animals; Chronic Pain; chronic pain; metabolism

Pain often persists in patients with an inflammatory disease, even when inflammation has subsided. The molecular mechanisms leading to this failure pain resolution and the transition chronic are poorly understood. Mitochondrial dysfunction sensory neurons links pain, but its role of is unclear. Transient causes neuronal plasticity, called hyperalgesic priming, which impairs induced by a subsequent stimulus. We identify that priming mice increases expression mitochondrial protein (ATPSc-KMT) metabolic disturbances neurons. Inhibition respiration, knockdown ATPSCKMT expression, or supplementation affected metabolite sufficient restore prevents development. Thus, inflammation-induced mitochondrial-dependent predispose development pain.