Objective     To probe the occurrence of neuroal apoptosis in rats after status epilepticus (SE) and the relationship between neuron apoptosis and caspase-3 expression.      Methods     Rat model of SE was induced by intraperitoneal injection of 300 mg/kg pilocarpine in 20 male Wistar rats. Another 5 rats served as control. The apoptotic neuron was detected by TdT-mediated dUTP Nick End Labeling (TUNEL)

and caspase-3 expression was observed by immunocytochemistry at 6

th

48

th

72

th

h and 7

th

d after SE induction.      Results     In con

trol rats

TUNEL-positive neuron could not be found in hippocampus. The number of TUNEL-positive neuron began to increase at 6

th

h after SE induction and peaked at 72

th

h

began to decrease at 7

th

d after SE induction. In control rats

there were few caspase-3 expression in hippocampus. The caspase-3 immunoreactivity began to increase at 6

th

h after SE and peaked at 48

th

h

especially in CA1 and CA3 region of hippocampus

began to decrease at 72

th

h and dropped to normal level at 7

th

d. The results indicated that the distribution of caspase-3 expression was consistent with the distribution of TUNEL-positive neuron. The peak of caspase-3 expression was earlier than that of TUNEL-positive neuron.      Conclusion     Neuron apoptosis participated in the process of delayed neuronal death in hippocampus after SE and was correlated with caspase-3 activation.