The expression of c-fos protein was examined by means of immunocytochemistry in the rat brain following incomplete ischaemia, to elucidate the molecular mechanisms of post-ischaemic neuronal death and of the modulated neurotransmission of surviving neurons. Incomplete ischaemia was produced by permanent unilateral or bilateral common carotid artery (CCA) occlusion. After 1 h of unilateral occlusion, the level of c-fos protein-like nuclear immunoreactivity increased in cortical neurons ipsilateral to the insult, especially in cingulate and piriform cortices. The reactivity peaked at 3-6 h, and was undetectable after 3 days. A number of scattered immunostained neurons in the ipsilateral subiculum, CA 1 and dentate gyrus became visible after 1 day. The effect reached a peak between 1-3 days, then returned to basal levels by 7 days. Bilateral CCA occlusion showed a similar distribution of immunoreactivity, but on both hemispheres. Immunoreactive neurons were more numerous and intensely stained but more transient. The induction of c-fos was completely blocked or reduced by treatment with MK-801. Our results suggest that c-fos expression after CCA occlusion is NMDA receptor mediated, and that it has a specific role in neurons after ischaemic insult.
Animals Brain