Using a time-sharing fluorometer-reflectometer,
pyridine nucleotide (
NADH) and
flavoprotein (Fp) fluorescence, as well as reflected light at the excitation wavelength, were measured and correlated with the electrical activity of an awake cerebral cortex. Exposure of the rat to a
nitrogen atmosphere (
anoxia) led to an increase in signals representing the reduction of
pyridine nucleotides and
flavins, with very similar kinetics. Inducement of partial
ischemia by bilateral carotid artery
ligation led to an increase in
NADH, accompanied by a very small effect on the electrical activity (ECoG). In most animals, 2-3h after
ligation, the ECoG became flat or depressed. Exposure of this ischemic cerebral cortex to KC1
solution caused depression of the electrical activity without metabolic response probably due to the limitation of
oxygen supply. The metabolic state of an awake cerebral cortex was identified by exposing the brain to various levels of
oxygen, epileptoform activity, spreading depression, hyperbaric pressure of
oxygen and an uncoupler. From our results we conclude that the awake cerebral cortex is close to the resting state, state 4, rather than to the active state, state 3.