HYPOXIA POTENTIATES TRAUMATIC BRAIN INJURY-INDUCED EXPRESSION OF C-FOS IN RATS

HALOTHANE-anesthetized male rats were subjected to either moderately s evere parasagittal fluid percussion-induced traumatic brain injury (TB I) or sham injury, and for 30 min immediately after injury hypoxia was induced in half the rats from each group by substituting a 13% O-2, s ource to deliver halothane for continued anesthesia. At 60 min post-TB I, Northern blot analysis showed a significant increase in c-fos mRNA levels, by 60-100% above sham control levels in the frontal cortex, ce rebellum and hippocampus. Although hypoxia in sham-injured rats did no t by itself alter c-fos mRNA levels, it did significantly potentiate t he 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.