title: Hypoxia potentiates traumatic brain injury-induced expression of c-fos in rats.
abstract: Halothane-anesthetized male rats were subjected to either moderately severe parasagittal fluid percussion-induced traumatic brain injury (TBI) or sham injury, and for 30 min immediately after injury hypoxia was induced in half the rats from each group by substituting a 13% O2 source to deliver halothane for continued anesthesia. At 60 min post-TBI, Northern blot analysis showed a significant increase in c-fos mRNA levels, by 60-100% above sham control levels in the frontal cortex, cerebellum and hippocampus. Although hypoxia in sham-injured rats did not by itself alter c-fos mRNA levels, it did significantly potentiate the TBI-induced changes in c-fos mRNA in all three brain regions. These findings show that hypoxia is an important factor influencing genomic responses to TBI.
authors.affiliation: Division of Neurosciences, Walter Reed Army, Institute of Research, WRAMC, Washington, DC 20307-5100, USA.
authors.forename: J R
authors.initials: JR
authors.lastname: Dave
authors.forename: R A
authors.initials: RA
authors.lastname: Bauman
authors.forename: J B
authors.initials: JB
authors.lastname: Long
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000378:metabolism*; D004195:Disease Models, Animal; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger