CLINICAL NEUROSCIENCE AND NEUROPATHOLOGYc-fos expression and redox state of cytochrome oxidase of rat brain in hypoxiaNomura, Yasutomo1; Kinjo, Masataka1; Tamura, Mamoru1,2Author Information 1Laboratory of Supramolecular Biophysics, Research Institute for Electronic Science, Hokkaido University, Sapporo 060-0812 Japan 2Corresponding Author: Mamoru Tamura Received 6 October 1999; accepted 12 November 1999 Acknowledgments: This study was supported in part by Grants-in-Aid for Scientific Research on Priority Areas (A) (2) (11170201) and for Encouragement of Young Scientists (10780490) from the Ministry of Education Science, Sports and Culture of Japan. NeuroReport: February 7, 2000 - Volume 11 - Issue 2 - p 301-304 Buy Abstract Hypoxic induction of c-fos was studied in rat brains as a function of the cerebral oxygenation state using near-infrared spectroscopy by which the hemoglobin oxygenation state and redox state of mitochondrial cytochrome oxidase could be monitored noninvasively. Following reoxygenation after hypoxia, the expression of c-fos and MAP2 mRNAs was followed by reverse transcription-coupled PCR. The expression of MAP2 remained unchanged throughout all the conditions from 21 to 8% FiO2. Under mildly hypoxia conditions, c-fos mRNA was not induced. Hemoglobin was partially deoxygenated but cytochrome oxidase remained fully oxidized. Severe hypoxia, where cytochrome oxidase was reduced, caused a significant induction of c-fos mRNA. At this stage, the oxygen concentration in cerebral tissue fell to <10-7 M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA. © 2000 Lippincott Williams & Wilkins, Inc.