Objective  To investigate the neurogenetic function of Citalopram in rat hippocampus after transient cerebral ischemia and its effects on the animals’ cognitive function.   Methods  Totally 78 Wistar rats were randomly divided into four groups: normal control group (NC)

sham operation control group (SC)

transient cerebral ischemia group (4VO)

transient cere

bral ischemia group treated with Citalopram (4VO+C). The improved Pulsinelli’s 4-vessel occlusion was used to establish ischemia in rats. Neurogenesis in hippocampus was observed by BrdU (Bromodeoxyuridine) immunofluorescence and confocal laser scanning microscopy. The cognitive function of the rats was evaluated by Morris water maze test.   Results  Most of the BrdU-positive cells were detected in dentate gyrus

and generally in pairs or clusters

distributed at the border of the granule cell layer and hilus. One day after transient cerebral ischemia

the BrdU-positive cells obviously decreased in number in both 4VO and 4VO+C groups (P=0.002)

then gradually increased and reached the peak 14 days after operation; The number of BrdU-positive cells in 4VO+C group was twice as much as that in 4VO group. Besides

neurogenesis was vividly continued 21 days after operation in 4VO+C group (P0.01 compared with 4VO group). Both place navigation test and spatial probe test showed that the cognitive function was significantly injured by transient cerebral ischemia in 4VO group as well as in 4VO+C group rats. But as time went on

the cognitive function was improved. Furthermore the results of Morris water maze test were significantly better in 4VO+C group on 14

th

day and 21

st

day after operation than those corresponding results in 4VO group (P0.05). The tendency of neurogenesis in adult dentate gyrus had no significant correlation with the cognitive function of rats.   Conclusion  Transient cerebral ischemia established by Pulsinelli’s 4-vessel occlusion in rats could stimulate neurogenesis in adult dentate gyrus and could be improved by Citalopram. Citalopram relieves the cognitive injury induced by transient cerebral ischemia. The differentiation and integration of proliferated neural stem cells or function of neurotransmitter may contribute to no correlation between hippocampal neurogenesis and cognitive function.