Mitochondria constantly release various amounts of superoxide anions which are usually rapidly converted to H2O2. Especially disturbance of mitochondrial function can lead to an increased production rate of reactive oxygen species (ROS) and the resulting oxidative stress may induce cellular damage and cell death. By affecting the cellular redox state and modifying the activity of cysteine-containing proteins by means of sulfhydryl modulation, physiological and pathophysiological ROS generation is believed to take part in redox signaling. In this thesis the signaling function of cytosolic redox changes and the functional consequences for the intact hippocampal network were analyzed. The experiments were conducted on the network-level (acute hippocampal slices), single-cell-level (cultured neurons) and molecular-level. Extracellular application of H2O2 led to a rise of [Ca2+]i, obviously due to Ca2+ release from the ER via activation of ryanodine receptors. The mitochondrial membrane potential, synaptic function and cellular ATP-levels were however only barely affected. By utilizing the innovative redoxsensitive roGFP, dynamic measurements of the redox-state could be performed on the single-cell-level and the various mitochondrial activity parameters could be correlated systematically with the redox-state. Cytosolic redox state was modified by modulating mitochondrial respiration and this in turn affected the susceptibility of hippocampal slices to hypoxia. A pronounced mitochondrial depolarization by 1 µM FCCP or 1 mM NaCN markedly increased the susceptibility of hippocampal slices to hypoxia and even induced spreading depression (SD) episodes despite the presence of O2. An increase of endogenous superoxide- or hydroxyl radical-production also hastened the onset of a hypoxia-induced spreading depression (HSD). Surprisingly H2O2 (1 - 5 m M) postponed the onset of a HSD - obviously by mediating sulfhydryl ox idation - without impairing the viability of the slices tested, indicating a potential neuroprotective effect. The identification of further redoxsensitive targets involved is still pending. In view of a potential neuroprotection of sulfhydryl oxidation during metabolic disturbances this will be of highest clinical relevance.