IS C-JUN INVOLVED IN NERVE-CELL DEATH FOLLOWING STATUS EPILEPTICUS AND HYPOXIC-ISCHEMIC BRAIN INJURY

Neurons undergoing delayed neuronal death produced by hypoxia-ischaemi a (HI) or status epilepticus (SE) showed a massive expression of c-Jun in their nuclei 24 h after the insult. With SE there was also a weake r induction of c-Fos and Jun B in dying neurons. SE induced in the pre sence of the NMDA antagonist MK-801 produced no delayed c-Jun expressi on in the hippocampus and nerve cell death did not occur in this regio n, although there was a delayed c-jun expression in the amygdala/pirif orm region, and cell death occurred in this area. Activation of centra l muscarinic receptors with pilocarpine, or block of D2 dopamine recep tors with haloperidol, treatments which do not cause neuronal damage, strongly induced Fos and Jun B in hippocampal and striatal neurons, bu t only induced c-Jun very weakly. Thus, c-Jun may participate in the g enetic cascade of events that produce programmed cell death in neurons .