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dc.contributor.authorRenshaw, Gillianen_US
dc.contributor.authorNikinmaa, M.en_US
dc.contributor.editorAbel Lajtha and Dianna A Johnsonen_US
dc.date.accessioned2017-05-03T12:01:40Z
dc.date.available2017-05-03T12:01:40Z
dc.date.issued2007en_US
dc.date.modified2008-06-12T06:46:26Z
dc.identifier.isbn9780387303499en_US
dc.identifier.urihttp://hdl.handle.net/10072/19281
dc.description.abstractNeural systems exposed to diminished oxygen availability have a compromised metabolism that leads to pathophysiological changes or neuronal death, depending on the severity and duration of oxygen deprivation. A distributed network of oxygen sensors responds to protect cells by slowing or ameliorating pathophysiological changes and forestalling neuronal death via short-term or long-term changes involving gene expression and the modification of sensors and effectors. In mammalian systems such protective changes are not sufficient to prevent damage under extreme conditions, unlike some hypoxia and anoxia-tolerant vertebrates which demonstrate oxygen-dependent, reversible reprogramming to protect vital organs such as the brain and heart. This chapter examines (1) the nature of the signal for oxygen sensors; (2) the molecules used to sense oxygen; (3) how the primary signal is generated, converted, and used in an oxygen-dependent manner; (4) how effector systems function in different cell types; and (5) how oxygen sensing pathways are interconnected to more general protective stress responses which confer cross protection for a number of physiological stressors. While future therapies may focus on the activation of hypoxia inducible factor (HIF) and its downstream gene products, selected gene products could be administered to reduce neuronal loss and improve recovery after acute insults due to ischemic events and degenerative diseases of the brain and retina. Activation of neuroprotective pathways by oxygen sensors and other physiological stressors could be used as pre-treatment to minimize neurotrauma associated with neurosurgical procedures and as an ancillary treatment during early stages of rehabilitation.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.format.extent312735 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherSpringer-Verlagen_US
dc.publisher.placeGermanyen_US
dc.publisher.urihttp://www.springer.com/biomed/neuroscience/book/978-0-387-30349-9en_AU
dc.relation.ispartofbooktitleHandbook of Neurochemistry and Molecular Neurobiology: sensory neurochemistryen_US
dc.relation.ispartofchapter11en_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom271en_US
dc.relation.ispartofpageto296en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchcode320307en_US
dc.titleOxygen Sensors of the Peripheral and Central Nervous Systemsen_US
dc.typeBook chapteren_US
dc.type.descriptionB1 - Book Chapters (HERDC)en_US
dc.type.codeB - Book Chaptersen_US
gro.rights.copyrightCopyright 2007 Springer. The attached file is reproduced here in accordance with the copyright policy of the publisher. The original publication is available at www.springerlink.comen_AU
gro.date.issued2007
gro.hasfulltextFull Text


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