Journal
NATURE NEUROSCIENCE
Volume 20, Issue 5, Pages 700-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4526
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Funding
- National Heart, Lung, and Blood Institute of the NIH [RO1HL028785, RO1HL074011]
- National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health (NIH) [R01DK085259, R01DK062324]
- Japan Society for the Promotion of Science
- National Institutes of Health [1S10RR026799-01]
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C1 neurons, located in the medulla oblongata, mediate adaptive autonomic responses to physical stressors (for example, hypotension, hemorrhage and presence of lipopolysaccharides). We describe here a powerful anti-inflammatory effect of restraint stress, mediated by C1 neurons: protection against renal ischemia-reperfusion injury. Restraint stress or optogenetic C1 neuron (C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI). The protection was reproduced by injecting splenic T cells that had been preincubated with noradrenaline or splenocytes harvested from stressed mice. Stress-induced IRI protection was absent in Chrna7 knockout (a7nAChR(-/-)) mice and greatly reduced by destroying or transiently inhibiting C1. The protection conferred by C1 stimulation was eliminated by splenectomy, ganglionic-blocker administration or beta(2)-adrenergic receptor blockade. Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI protection persisted after subdiaphragmatic vagotomy or corticosterone receptor blockade. Overall, acute stress attenuated IRI by activating a cholinergic, predominantly sympathetic, anti-inflammatory pathway. C1s were necessary and sufficient to mediate this effect.
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