Stress, particularly social defeat stress, is known to activate mesocortical dopaminergic neurons in a manner correlated with increased depressive-like phenotypes in laboratory rodents. As an immediate early gene, it is not surprising that this increased activation might lead to an increase in c-fos in neurons within this pathway, and this has been observed (see for example Tanaka et al. 2012 in the Journal of Neuroscience). To my knowledge, a global elevation of c-fos has not been observed in association with depression phenotypes. Neuronal hyperactivity (among excitatory pyramidal cells) in pathological states such as epilepsy does show a more widespread activation although the increase generally occurs to a greater extent in some local focal region (for instance, in the hippocampus for temporal lobe epilepsy models). If you mean spreading depression, the neurological phenomenon in which suppressed activity occurs in a travelling wave across cortical regions not the psychiatric disorder, there is some evidence that c-fos is activated particularly when the pathological response is initiated by traumatic brain injury. Herrera and Robertson's 1996 review in progress in neurobiology provides a good reference describing many early observations of changes in c-fos expression under different conditions in experimental animals.