OBJECTIVE: To explore the effects ginkgo diterpene ginkgolides（DG） on cognitive function of immature rats anesthetized by ketamine. METHODS: Fifty immature SD rats were randomly divided into the control group（Con）

ketamine group（Ket）

DG low-dose group（DG-L

2.5 mg/kg）

DG medium-dose group（DG-M

5 mg/kg） and DG high-dose group（DG-H

10 mg/kg）. The rats in non-control group were anesthetized with 100 mg/kg ketamine for cognitive dysfunction model. Different doses of DG were intraperitoneally injected. Morris water maze was used to detect cognitive function

long-term potential was used to detect synaptic plasticity

Golgi stain was used to detect the state of dendritic spines

Western Blot was used to detect the expression of brain-derived neurotrophic factor（BDNF）

TrkB and PSD-95 protein. RESULTS: Compared with the Con group

ketamine anesthesia（Ket group

DG-L

DG-M and DG-H） resulted in increased escape latency

decreased number of crossing platforms

decreased density and length of mediated dendritic spines

down-regulated excitatory postsynaptic field potential（fEPSP） level

and decreased expression of BDNF

TrkB and PSD-95 proteins in the hippocampus

decreased B-cell lymphoma 2（Bcl-2） expression

increased cleaved-caspase-3 and Bcl-2 associated X protein（Bax） expression. Compared with the Ket group

the escape latency of immature rats in the DG-M and DG-H was significantly shortened

the number of crossing platforms increased

the growth of dendritic spines was promoted

the level of fEPSP was up-regulated

the protein expressions of BDNF

TrkB and PSD-95 increased

and Bcl-2 expression increased

and the cleaved-caspase-3 and Bax expression decreased. CONCLUSIONS: By increasing the protein expression of BDNF

TrkB and PSD-95

DG reduces the ketamine-induced dendritic spine injury in immature rats

up-regulates the fEPSP

and improves the cognitive impairment in immature rats.