Oxygen sensing neurons and neuropeptides regulate survival after anoxia in developing C. elegans

• Published in: PloS one Vol. 9; no. 6; p. e101102
• Main Authors: Flibotte, John J, Jablonski, Angela M, Kalb, Robert G
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 26.06.2014; Public Library of Science (PLoS)
• Subjects: Ablation; Analysis; Animals; Animation; Anoxia; Biology and Life Sciences; Brain; Brain injuries; Brain injury; Caenorhabditis elegans; Caenorhabditis elegans - metabolism; Caenorhabditis elegans Proteins - metabolism; Cell cycle; Cell survival; Circuits; Detection; Enzyme Activation; Experiments; Guanylate Cyclase - metabolism; Head injuries; Heat-Shock Response; Hypoxia; Hypoxia - metabolism; Infants; Medical research; Medicine and Health Sciences; Nematodes; Neurodevelopmental disorders; Neurons; Neurons - metabolism; Neuropeptides; Neuropeptides - metabolism; Neurosciences; Oxygen; Oxygen - metabolism; Pediatrics; Phenotype; Premature infants; Receptor, Insulin - metabolism; Research and Analysis Methods; Sensitivity; Signal Transduction; Signaling; Survival; Traumatic brain injury; Worms
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0101102

Hypoxic brain injury remains a major source of neurodevelopmental impairment for both term and preterm infants. The perinatal period is a time of rapid transition in oxygen environments and developmental resetting of oxygen sensing. The relationship between neural oxygen sensing ability and hypoxic injury has not been studied. The oxygen sensing circuitry in the model organism C. elegans is well understood. We leveraged this information to investigate the effects of impairments in oxygen sensing on survival after anoxia. There was a significant survival advantage in developing worms specifically unable to sense oxygen shifts below their preferred physiologic range via genetic ablation of BAG neurons, which appear important for conferring sensitivity to anoxia. Oxygen sensing that is mediated through guanylate cyclases (gcy-31, 33, 35) is unlikely to be involved in conferring this sensitivity. Additionally, animals unable to process or elaborate neuropeptides displayed a survival advantage after anoxia. Based on these data, we hypothesized that elaboration of neuropeptides by BAG neurons sensitized animals to anoxia, but further experiments indicate that this is unlikely to be true. Instead, it seems that neuropeptides and signaling from oxygen sensing neurons operate through independent mechanisms, each conferring sensitivity to anoxia in wild type animals.